Autoimmunity And Autoimmune Disease Notes

Autoimmune mechanisms underline many diseases, some organ-specific, others systemic in distribution.

Autoimmune disorders can overlap: an individual may have more than one organspecific disorder;or more than one systemic disease.

Genetic factors such as HLA type are important in autoimmune disease, and it is probable that each disease involves several factors.

Autoimmune mechanisms are pathogenic in experimental and spontaneous animal models associated with the development of autoimmunity.

Human autoantibodies can be directly pathogenic.

Immune complexes are often associated with systemic autoimmune disease.

Autoreactive B and T cells persist in normal subjects but in disease are selected by autoantigen in the production of autoimmune responses.

Microbial cross-reaching antigens and cytokine dysregulation can lead to autoimmunity.

Autoantibody tests are valuable for diagnosis and sometimes for prognosis.

Treatment of organ-specific diseases usually involves metabolic control.
Treatment of systemic diseases includes the use of anti-inflammatory and immunosuppressive drugs.

Future treatment will probably focus on manipulation of the pivotal auto reactive T cells by antigens or peptides, by anti CD4 and possibly T cell vaccination.


The immune system has tremendous diversity and because the repertoire of specificities express by the B- and T-cell populations is generated randomly, it is bound to include many which are specific for self components. Thus the body must establish self-tolerance mechanisms, to distinguish between self and non-self determinants, so as to avoid auto reactivity (see Chapter 7). However, al mechanism has a risk of breakdown. The self recognition mechanisms are no exception, and a number of disease have been identified in which there is autoimmunity, due to copious production of autoantibodies and auto reactive T cells. One of the earliest examples in which the production of autoantibodies was associated with disease in a given organ is Hashimoto’s thyroiditis. Among the autoimmune diseases, thyroiditis has been particularly well-studied, and many of the aspects discussed in this chapter will draw upon our knowledge of it. It is a disease of the thyroid which is most common in middle-aged women and often lead to formation of a goiter and hypothyroidism.

The gland is infiltrated, sometimes to an extraordinary extent, with inflammatory lymphoid cells.

These are predominantly mononuclear phagocytes, lymphocytes and plasma cells, and secondary lymphoid follicles are common (Figure-1). In Hashimoto’s disease, the gland often shows regenerating thyroid follicles but this is not a feature of the thyroid in the related condition, primary myxoedema, in which comparable immunology features are seen and where the gland undergoes
almost complete destruction and shrinks. The serum of patients with Hashimoto’s disease usually contains antibodies to thyroglobulin. These antibodies are demonstrable by agglutination and by precipitin reactions when present in high titre. Most patients also have anti bodies directed against a
cytoplasmic or microsome antigen, also present on the apical surface of the follicular epithelial cells (Figure-2), and now known to be thyroid peroxidase, the enzyme which iodinates thyroglobulin.


The antibodies associated with Hashimoto’s thyroiditis and primary myxoedema react only with the thyroid, so the resulting lesion is highly localized. By contrast, the serum from patients with diseases such as systemic lupus crythematosus (SLE) reacts with many, if not all, of the tissues I the body. In SLE, one of the dominant antibodies is directed against the cell nucleus (Figure-2). These two diseases represent the extremes of the autoimmune spectrum (Figure-3). The common target organs in organ-specific disease include the thyroid, adrenals, stomach and pancreas. The non-organ-specific diseases, which include the rheumatological disorders, characteristically involve the skin, kidney, joints and muscle (Figure-4).

An individual may have more then one autoimmune disease

Interestingly, there are remarkable overlaps at each end of the spectrum. Thyroid antibodies occur with a high frequency in pernicious anaemia patients who have gastric autoimmunity, and these patients have a higher incidence of thyroid autoimmune disease than the normal population.

Similarly, patients with thyroid autoimmunity have a high incidence of stomach autoantibodies and, to a lesser extent, the clinical disease itself, namely pernicious anaemia. The cluster of hematological disorders at the other end of the spectrum also shows considerable overlap. Features of rheumatoid
arthritis, for example, are often associated with the clinical picture of SLE. In these diseases immune complexes are deposited systemically, particularly in the kidney, joints and skin, giving rise to widespread lesions. By contrast, overlap of diseases from the two ends of the spectrum is relatively
rare. The mechanisms of immunopathological damage vary depending on where the disease lies in the spectrum. Where the antigen is localized in a particular organ, Type II hypersensitivity and cell-mediated reactions are most important. In non-organ-specific autoimmunity, immune complex deposition leads to inflammation through a variety of mechanisms, including complement activation and phagocyte recruitment.


Autoimmune disease can occur in families

There is an undoubted family incidence of autoimmunity. This is largely genetic rather than environmental, as many be seen from studies of identical and non-identical twins, and from the associated of thyroid autoantibodies with abnormalities of the Xchromosome. Within the families of patients with organ-specific autoimmunity, not only is there a general predisposition to develop organ-specific antibodies, it is also clear that other genetically controlled
factors tend to select the organ that is mainly affected. Thus, although relatives of Hashimoto patients and families of pernicious anaemia patients both have higher than normal incidence and titer of thyroid autoantibodies, the relatives of pernicious anaemia patients have a far higher frequency of gastric autoantibodies, indicating that there are genetic factors which differentially
select the stomach as the target within these families.

Certain HLA Haplotypes Predispose To Autoimmunity

Further evidence for the operation of genetic factors in autoimmune disease comes from their tendency to be associated with particular HLA specificities (Figure-5). Rheumatoid arthritis shows no associations with the HLA-A and-B loci haplotypes, but is associated with a nucleotide sequence (encoding amino
acids 70-74 in the DRβ chain) that is common to DR1 and major subtypes of DR4.

This sequence is also present in the dnaJ heat-shock proteins of various bacilli and EBV gp 110 proteins, presenting an interesting possibility for the induction of autoimmunity by a microbial cross-reacting epitope (see below). The plot gets even deeper, though, with the realization that HLA-DR molecules bearing this sequence can bind to another bacterial heat shock protein, dna K, and to the human analogue, namely hsp73, which targets selected proteins to lysosomes for antigen processing. The haplotype B8, DR3 is particularly common in the organ specific diseases, although Hashimoto’s thyroiditis tends to be associated more with DR5. It is notable that for insulin-dependent (type 1) diabetics mellitus, DQ2/8 heterozygotes have a greatly increased risk of
developing the disease (Figure-5). Although HLA risk factors tend to dominate-wide searches for mapping the genetic intervals containing genes for predisposition to disease by linkage to micro satellite markers (polymorphic variable numbers of tandem repeats, VNTR) reveal a plethora of genes affecting loss of tolerance, sustained inflammatory responses and end-organ targeting.


Autoimmune processes are often pathogenic. When autoantibodies are fond in association with a particular disease there are three possible inferences:
• The autoimmunity is responsible for producing the lesions of the disease.

• There is a disease process which, through the production of tissue damage, leads to the development of autoantibodies.

• There is a factor which produces both the lesions and the autoimmunity. Autoantibodies secondary to a lesion (the second possibility) are sometimes found. For example, cardiac autoantibodies may develop after myocardial infarction. However, sustained production of autoantibodies rarely follows the release of autoantigens by simple trauma. In most diseases associated with autoimmunity, the evidence supports the first possibility, that the autoimmune
process produces the lesions.

The pathogenic role of autoimmunity can be demonstrated in experimental models

Examples of induced autoimmunity

The most direct test of whether autoimmunity is responsible for the lesions of disease is to induced autoimmunity deliberately in an experimental animal and see if this leads to the production of the lesions. Autoimmunity can be induced in experimental animals by injecting auto antigen (self antigen) together with complete Freund’s adjuvant, and this does indeed produce organ-specific
disease in certain organs. For example, thyroglobulin injection can induce an inflammatory disease of the thyroid while myelin basic protein can cause encephalomyelitis. In the case of thyroglobulin-injected animals, not only are thyroid autoantibodies produced, but the gland becomes infiltrated with mononuclear cells and the acinar architecture crumbles, closely resembling the histology of Hashimoto’s thyroiditis. The ability to induce experimental autoimmune disease depends on the strain of animal used.

For example, it is found that the susceptibility of rats and mice to myelin basic protein-induced encephalomyelitis depends on a small number of gene loci, of which the most important are the MHC class II genes. The disease can be induced in susceptible strains by injecting T cells belong to the CD4/TH1 subset and it has been found that induction of disease can be prevented by treating
the recipients with antibody to CD4 just before the expected time of disease onset, blocking the interaction of the TH cells’ CD4 with the class II MHC of antigen-presenting target cells. The results indicate the importance of class II restricted auto reactive TH cells I the development of these conditions, and emphasize the prominent role of the MHC.

Examples of spontaneous autoimmunity

It has proved possible to breed strains to animals which are genetically programmed to develop autoimmune diseases closely resembling their human counterparts. One well established example is the Obese strain (OS) chicken (Figure-6) which parallels human autoimmune thyroid disease in terms
of the lesion in the gland, the production of antibodies to different components in the thyroid, and the overlap with gastric autoimmunity. So it is of interest that when the immunological status of these animals is altered, quite dramatic effects on the outcome of the disease are seen.

For example, removal of the thymus at birth appears to exacerbate the thyroiditis, suggesting that the thymus exerts a controlling effect on the disease, but if the entire T-cell population is abrogated by combining thymectomy with massive injections of anti-chick T-cell serum, both autoantibody production and the attack on thyroid are completely inhibited. Thus, T cells play a variety of pivotal roles as mediators and regulators of this disease. The non-obese diabetic (NOD) mouse provides an excellent model for human insulin-dependent diabetes mellitus (IDDM; type 1 diabetes) where the
insulin producing β cells of the pancreatic islets of Langerhans are under attack from a chronic leukocytic infiltrate of T cells and macrophages (Figure-7). The role of the T cells in mediating this attack is evident from the amelioration and prevention of disease by treatment of the mice with a non-depending anti-CD4 monoclonal antibody, which in the presence of the pancreatic auto-antigens, insulin and glutamic acid decarboxylase (GAD) induces specific T cell anergy.
The dependence of yet another spontaneous model, the F1 hybrid of New Zealand Black and White strains (NZB x W/F1), on the operation of immunological processes is aptly revealed by the suppression of the murine SLE which characterizes this strain, by treatment with anti-CD4 (Figure-8).

Human autoantibodies can be directly pathogenic

When investigating human autoimmunity directly, rather than using animal models, it is of course more difficult to carry out experiments. Nevertheless, there is much evidence to suggest that autoantibodies may be important in pathogenesis, and we will discuss the major examples here.

Thyroid autoimmune disease – A number of disease have been recognized in which autoantibodies to hormone receptors may actually mimic the function of the normal hormone concerned and produce disease. Graves’ disease (thyrotoxicosis) was the first disorder in which such anti-receptor antibodies were clearly recognized. The phenomenon of neonatal thyrotoxicosis provides us with a natural ‘passive transfer’ study, because the IgG antibodies from the thyrotoxic mother cross the placenta and react directly with thyroid stimulating hormone (TSH) receptor o the neonatal thyroid.

Many babies born to thyrotoxic mothers and showing thyroid hyperactivity have been reported, but the problem spontaneously resolves as the antibodies derived from the mother are catabolized in the baby over several weeks. Whereas autoantibodies to the TSH receptor may stimulate cell division and/or increase the production of thyroid hormones, others can bring about the opposite effect by inhibiting these functions, a phenomenon frequently observed in the receptor responses to ligands which act as agonists or antagonists. Different combinations of the various manifestations of
thyroid autoimmune disease, chronic inflammatory cell destruction and stimulation or inhibition of growth and thyroid hormone synthesis, can give rise to a wide spectrum of clinical thyroid dysfunction (Figure-9).

Myasthenia gravis – A parallel with neonatal hyperthyroidism has been observed with mothers suffering from myasthenia gravis, where antibodies to acetylcholine receptors cross the placenta into the fetus and may cause transient muscle weakness in the newborn baby.

Other receptor diseases – Somewhat rarely, autoantibodies to insulin receptors and to βadrenergic receptors can be found, the latter associated with bronchial asthma. Neuromuscular defects can be elicited in mice injected with serum from patients with the Lambert – Eaton syndrome containing antibodies to presynaptic calcium channels, while sodium channel autoantibodies have been identified in the Guillain – Barre syndrome.

Male infertility – Yet another example of autoimmune disease is seen in rate cases of male infertility were antibodies to spermatozoa lead to clumping of spermatozoa, either by their heads or by their tails, in the semen.

Pernicious anaemia – In this disease an autoantibody interferes with the normal uptake of vitamin B12.Vitamine B12 is not absorbed directly, but must first associated with a protein called intrinsic factor; the vitamin-protein complex is then transported across the intestinal mucosa. Early passive transfer studies demonstrated that serum from a patient with pernicious anaemia, if fed to a healthy individual together with intrinsic factor – B12 complex, inhibited uptake of the vitamin.

Subsequently, the factor in the serum which blocked vitamin uptake was identified as antibody against intrinsic factor. It is now known that plasma cells in the gastric mucosa of patients with pernicious anaemia secrete this antibody into the lumen of the stomach (Figure-10).

Goodpasture’s syndrome – In goodpasture’s syndrome, antibodies to the glomerular capillary basement membrane bind to the kidney in vivo (Figure-3). To demonstrate that the antibodies can have a pathological effect, a passive transfer experiment was performed. The antibodies were eluted from the kidney of a patient who had died with this disease, and injected into primates whose kidney antigens were sufficiently similar for the injected antibodies to localize on the glomerular basement membrane. The injected monkeys subsequently died with glomerulonephritis.

Blood and vascular disorders – Autoimmune haemolytic anaemia and idiopathic thrombocytopenia purpura result from the synthesis of autoantibodies to red cells and platelets, respectively. The
primary antiphospholipid syndrome characterized by recurrent thromboembolic phenomena and feta loss is triggered by the reaction of autoantibodies with a complex of β2-glycoprotein turns up again as an abundant component of atherosclerotic plaques and there is increasing attention to the idea that autoimmunity may initiate or exacerbate the process of lipid deposition and plaque formation in this disease, the two lead candidate antigens being heat-shock protein 60 and the low- density lipoprotein, apoprotein B. The necrotizing granulomatous vasculitis which characterizes
Wegener’s granulomatosis is associated with antibodies to neutrophil cytoplasmic proteinase III (cANCA) but their role in pathogenesis of the vaculitis is ill defined.

Immune Complexes appear to be pathogenic in systemic autoimmunity

In the case of SLE, it can be shown that complement-fixing complexes of antibody with DNA and other nucleosome components such as histones are deposited in the kidney (Figure-3), skin, joints and choroid plexus of patients, and must be presumed to produce Type III hypersensitivity reactions.
Cationic anti-DNA antibodies and histones facilitate the binding to heparin sulphate in the connective tissue structures. Individuals with genetic deficiency of the early classical pathway complement components clear circulating immune complexes very poorly and are unduly susceptible to the development of SLE. Turing to the experimental models, we have already mentioned the (NZB x W) F1 which spontaneously develops murine SLE associated with immune-complex glomerulonephritis and anti-DNA autoantibodies as major features. The fact that measures which suppress the immune response in these animals (e.g. treatment with azathioprine or anit-CD4) also suppress the disease and prolong survival, adds to the evidence for autoimmune reactions causing such disease (Figure-8).

The erosions of cartilage and bone in rheumatoid arthritis are mediated by macrophages and fibroblasts which become stimulated by cytokines from activated T cells and immune complexes generated by a vigorous immunological reaction within the synovial tissue. The complexes can arise
through the self-association of IgG rheumatoid factors specific for the Fcy domains, a process facilitated by the striking deficiency of terminal galactose on the biantennary N-linked Fc iligosaccharides (Figure-11). This agalacto glycoform of IgG in complexes can exacerbate inflammatory reactions through reaction with mannosebinding lectin and production of TNE.

Evidence for directly pathogenic T cells in human autoimmune disease is hard to get

Adoptive transfer studies have shown that TH1 cells are responsible for directly initiating the lesions in experimental models of organ-specific autoimmunity. In the human, the production of high affinity, somatically mutated IgG autoantibodies characteristic of Tdependent responses, the isolation of thyroid-specific T-cell clones from the glands of Graves’ disease patients, the beneficial effect of cyclosporine in pre-diabetic individuals and the close association with certain HLA haplotypes, make it abundantly clear that T cells are utterly pivotal for the development of autoimmune disease. However, it is difficult to identify a role for the T cell as a pathogenic agent as
distinct from a T-helper function in the organ-specific disorders. Indirect evidence from circumstances showing that antibodies themselves do not cause disease, such as in babies born to mothers with insulin-dependent diabetes (IDDM), may be indicative.

Autoimmunity is antigen driven

Given that auto-reactive B cells exist, the question remains whether they are stimulated to proliferate and produce autoantibodies by interaction with auto-antigens or by some other means, such as non-specific polyclonal activators or idiotypic interactions (Figure-14). Evidence that B cells are selected by antigen comes from the existence of high affinity autoantibodies which arise through
somatic mutation, a process which requires both T cells and autoantigen.

Additionally, autoantibodies to epitope clusters occur on the same auto-antigenic molecule. Apart from the presence of auto-antigen itself, it is very difficult to envisage a mechanism that could account for the co-existence of antibody responses to different epitopes on the same molecule. A similar argument applies to the induction, in a single individual, of autoantibodies to organcelles (e.g. nucleosomes and spliceosomes which appear as belbs on the surface of apoptotic cells) or antigens linked within the same organ (e.g. thyroglobulin and thyroid peroxidase).

The most direct evidence for autoimmunity being antigen driven comes from studies of the Obese strain chicken which, as described earlier, spontaneously develops thyroid autoimmunity. If the thyroid gland (the source of antigen) is removed at birth, the chickens mature without developing
thyroid autoantibodies (Figure-13). Furthermore, once thyroid autoimmunity has developed, later removal of the thyroid leads to a gross decline of thyroid autoantibodies, usually to undetectable levels. Comparable experiments have been carried out in the non-obese diabetic (NOD) mouse which models human autoimmune diabetes; chemical destruction of the β cells leads to decline in
pancreatic autoantibodies. DNase treatment of lupus mice ameliorates the disease, presumably by destroying potentially pathogenic immune complexes.

In organ-specific disorders, there is ample evidence for T cells responding to antigens present in the organs under attack. But in non-organ-specific autoimmunity, identification of the antigens recognized by T cells is often inadequate. True, histone-specific T cells are generated in SLE patients
and histone could pay a ‘piggy back’ role in the formation of anti-DNA antibodies by substituting for natural antibody in the mechanism outlined in Figure-14. Another possibility is that the T cells do not see conventional peptide antigen (possibly true of anit-DNA responses) but instead recognize an
antibody’s idiotype (an antigenic determinant on the V region of antibody). In this view SLE, for example, might sometimes be initiated as an ‘idiotype disease’, like the model presented in Figure-14 In this scheme, autoantibodies are produced normally at low levels by B cells using germ-line genes. If these then form complexes with the autoantigen, the complexes can be taken up by APCs (including B cells) and components of the complex, including the antibody idiotype, presented to T cells. Idiotype-specific T cells would then help the autoantibody-producing B cells. Evidence for the induction of anti-DNA and glomerulonephritis by immunization of mice with the idiotype of germ-line ‘natural’ antiDNA autoantibody lends credence to this hypothesis.

Controls on the development of autoimmunity can be bypassed in a number of ways

Molecular mimicry by cross-reactive microbial antigens can stimulate autoreactive B and T cells

Normally, naïve autoreactive T cells recognizing cryptic self epitopes are not switched on because the antigen is only presented at low concentrations on ‘professional’ APCs or it may bepresented on ‘non-professional’ APCs such as pancreatic β-islet cells or thyroid epithelial cells, which lack B7 or other co-stimulator molecules. However, infection with a microbe bearing antigens that cross-react with the cryptic self epitopes (i.e. have shared epitopes) will load the professional APCs with levels of processed peptides that are sufficient to activate the naïve autoreactive T cells. Once primed, these T cells are able to recognize and react with the self epitope on the non-professional APCs since they no longer require a co-stimulatory signal and have a higher avidity for the target, due to upregulationof accessory adhesion molecules (Figure-15). 

Cross reactive antigens which share B cell epitopes with self molecules can also break tolerance but by a different mechanism. Many autoreactive B cells cannot be activated because the CD4+ helper T cells which they need are unresponsive either because these helper T cells are tolerized at lower concentration of autoantigens than the B cells or because they only recognize cryptic epitopes. However, these ‘helpless’ B cells can be stimulated if the cross-reaching antigen bears a ‘foreign’ carrier epitope to which the T cells have not been tolerized (Figure-16). The autoimmune process may persist after clearance of the foreign antigen if the activated B cells now focus the autoantigen on their surface receptors and present it to normally resting autoreactive T cell which will then proliferate and act as helpers for fresh B-cell stimulation.

A disease in which such molecular mimicry operates is rheumatic fever, in which autoantibodies to heart valve antigen can be detected. These develop in a small proportion of individuals several weeks after a streptococcal infection of the throat. Carbohydrate antigens on the streptococci cross-react with an antigen on heart valves, so the infection may bypass T-cell self tolerance to heart valve antigens. Shared B-cell epitopes between Yersinia enterolytica and the extracellular domain of the TSH receptor have recently been described. There may also be cross reactivity between HLA-B27 and certain strains of Klebsiella in connection with ankylosing spondylitis, and crossreactivity between bacterial heat-shock proteins and DR4 in relationship to rheumatoid arthritis. 

In this connection, it has been suggested that because processed MHC molecules may represent a major fraction of the peptide emitopes presented to differentiating T cells within the thymus, a significant proportion of positively selected cell which escape negative selection and enter the periphery will be specific for weakly binding cryptic MHC epitopes. One might therefore expect autoimmune responses to arise not infrequently through activation of these cells by molecular mimicry.

In some cases foreign antigen can directly stimulate auto-reactive cells 

Another mechanism to bypass the tolerant autoreactive TH cell is where antigen or another stimulator directly triggers the autoreactive effector cells. For example, lipopolysaccharide or Epstein-Barr virus causes direct B-cell stimulation and some of the clones of activated cells will produce autoantibodies, although in the absence of T-cell help these are normally of low titer and affinity. However, it is conceivable that an activated B cell might pick up and process its cognate autoantigen and present it to a naïve autoreactive T cell. 

Cytokine dysregulation, inappropriate MHC expression and failure of suppression may induce autoimmunity 

It appears that dysregulation of the cytokine network can also lead to activation of autoreactive T cells. One experimental demonstration of this is the introduction of a transgene for interferon-γ (IFNγ) into pancreatic β-islet cells. If the transgene for IFNγ is fully expressed in the cells, MHC class II genes are upregulated and autoimmune destruction of the islet cell results (Figure-17). This is not simply a result of a nonspecific chaotic IFNγ-induced local inflammatory milieu since normal islets grafted at a separate site are rejected, implying clearly that T-cell autoreactivity to the pancreas has been established.

The surface expression of MHC class II in itself is not sufficient to activate the naïve autoreactive T cells but it may be necessary to allow a cell to act as a target for the primed autoreactive TH cells, and it was therefore most exciting when cells taken from the glands of patients with Graves’ disease were found to be actively synthesizing class II MHC molecules (Figure-18) and so were able to be recognized by CD4+ T cells. In this context it is interesting that isolated cells from several animal strains that are susceptible to autoimmunity are also more readily induced by IFNγ to express MHC class II than are cells from non-susceptible strains. 

The argument that imbalanced cytokine production may also contribute to autoimmunity receives further support from the unexpected finding that tumour necrosis factor (introduced by means of a TNF transgene) ameliorates autoimmune disease in NZB x NZW hybrid mice. 

Aside from the normal ‘ignorance’ of cryptic self-epitopes, other factors which normally restrain potentially autoreactive cells may include regulatory T cells, hormones (e.g. steroids), cytokines (e.g. TGFβ) and products of macrophages (Figure-19). Deficiencies in any of them may increase susceptibility to autoimmunity. The feedback loop on Thelpersand macrophages through the pituitary – adrental axis is particularly interesting, as defects at different stages in the loop turn up in a variety of autoimmune disorders Figure-20). For example, patients with rheumatoid arthritis have low circulating corticosteroid levels compared with controls, and after surgery, although they produce copious amounts of IL-1 

and IL-6, a defect in the hypothalamic paraventricular nucleus prevents the expected increase in ACTH and adrenal steroid output. A subset of CD4 regulatory cell present in young healthy mice of the NOD strain can prevent the transfer of disease by spleen cells of diabetic animals to NOD mice congenic for the severe combined immunodeficiency trait; this regulatory subset is lost in older mice.

Pre-existing defects in the target organ may increase susceptibility to autoimmunity

We have already alluded to the undue sensitivity of target cells to upregulation of MHC class II by IFNγ in animals susceptible to certain autoimmune disease: Other evidence also favours the view that there may be a pre-existing defect in the target organ. In the Obese strain chicken model of spontaneous thyroid autoimmunity, not only is there a low threshold of IFNγ induction of MHC class II expressin by thyrocytes but it has also been shown that, when endogenous TSH is suppressed by thyroxine treatment, the uptake of iodine into the thyroid glands is far higher in the Obese strain than in a variety of normal strains. Furthermore, this is not due to any stimulating animals show even higher uptakes of iodine (Figure-21). Interestingly, the Cornell strain (from which the Obese strain was derived by breeding) shows even higher uptakes of iodine, yet these animals do not develop spontaneous thyroiditis. This could be indicative of a type of abnormal thyroid behavior which in itself is insufficient to induce autoimmune disease but does contribute to susceptibility in the Obese strain. Other situations in which the production of autoantigen is affected are diabetes, in which one of the genetic risk factors is associated with a microsatellite marker lying within a transcription factor controlling the rate of insulin production, and rheumatoid arthritis, in which the agalacto IgG glycoform is abnormally abundant. The intriguing observations that immunization atherosclerotic lesions at classical predilection sites object to major haemodynamic stress and that patients with atherosclerosis produce antibodies to human hsp60 which react with heat or IFNα-stressed endothelial cells, hints strongly at an autoimmune contribution to the pathology of the disease. Particularly relevant to the present discussion is the finding of upregulated hasp60 expression at such critical sites even in a 5-month-old child (Figure22). Again, one must re-emphasize the considerable importance of multiple factors I the establishment of prolonged autoimmunity.


Wherever the relationship of autoantibodies to the disease process, they frequently provide valuable markers for diagnostic purposes. A particularly good example is the test for mitochondrial antibodies, used in diagnosing primary biliary cirrhosis (Figure-23). Exploratory laparotomy was previously needed to obtain this diagnosis, and was often hazardous because of the age and condition of the patients concerned. Autoantibodies often have predictive value. For instance, individuals testing positively for antibodies to both insulin and glutamic acid decarboxylase have a high risk of developing insulin-dependent diabetes.


Often, in organ-specific autoimmune disorders, the symptoms can be conrolled by administration of thyroxine, and thyrotoxicosis by antithyroid drugs. In pernicious anaemia, 

metabolic correction is achieved by injection of vitamin B12, and in myasthenia gravis by administration of cholinesterase inhibitors. If the target organ is not completely destroyed, it may be possible to protect the surviving cells by transfection with FasL or TGFβ genes. Where function is completely lost and cannot be substituted by hormones, as many occur in lupus nephritis or chronic rheumatoid arthritis, tissue grafts or mechanical substitutes may be appropriate. In the case of tissue grafts, protection from the immunological processes which necessitated the transplant may be required.

Conventional immunosuppressive therapy with antimitotic drugs at high doses can be used to dam down the immune response but, because of the dangers involved, tends to be used only in life-threatening disorders such as SLE and dermatomyositis. The potential of cyclosporine and related drugs such as rapamycin has yet to be fully realized, but quite dramatic results have been reported in the treatment of type 1 diabetes mellitus. Anitinflammatory drugs are, of course, prescribed for rheumatoid diseases with the introduction of selective cyclo-oxygenase-2 (COX-2) inhibitors representing a welcome development. Encouraging results are being obtained by treatment of rheumatoid arthritis patients with low steroid doses at an early stage to correct the apparently defective production of these corticosteroids by the adrenal feedback loop, and for those with more established disease, attention is now focused on the striking remissions achieved by synergistic treatment with anti-TNFα monoclonals plus methotrexate.

As we understand more about the precise defects, and learn how to manipulate the immunological status of the patient, some less well-established approaches may become practicable (Figure-24). Several centres are trying out autologous stem-cell transplantation following haemato-immunoablation with cytotoxic drugs in severe cases of SLE, scleroderma and rheumatoid arthritis. Draconian reduction in the T cells in multiple sclerosis by Campath-1H (anti-CD52) and of the B-cell population with antiCD20 in rheumatoid arthritis are both under scrutiny. Treatment with Campath-1H followed by a non-depleting anti-CD4 has produced excellent remissions in patients with Wegener’s granulomatosis who were refractory to normal treatment. In an attempt to establish antigenspecific suppression, considerable clinical improvement has been achieved in exacerbating remitting multiple sclerosis by repeated injection of Cop 1, a random copolymer of alanine, glutamic acid, lysine and tyrosine meant to simulate the postulated ‘guilty’ autoantigen, myelin basic protection. Some experimental autoimmune disease have been treated successfully by feeding antigen to induce oral tolerance, by the inhalation of autoantigenic peptides and their analogues (Figure-25), and by ‘vaccination’ with peptides from heat-shock protein 70 or the antigen-specific receptor or autoreactive T cells. This suggests that stimulating normally suppressive functions, including the idiotype network, could be promising.

CRITICAL THINKING: Autoimmunity and autoimmune disease

Miss Jacob, a 30-year-old Caribbean lady, was seen in a rheumatology clinic with stiff painful joints in her hands, which were worse first thing in the morning. Other symptoms included fatigue, a low-grade fever, a weight loss of 2 kg, and some mild chest pain. Miss Jacob had recently returned to the UK from a holiday in Jamaica and was also noted to be taking the combined oral contraceptive pill. Past medical history of note was a mild autoimmune haemolytic anaemia 2 years previously. On examination Miss Jacob had a non-specific maculopapular rash on her face and chest and patchy alopecia (hair loss) over her scalp. Her mouth was tender and examination revealed an ulcer on the soft palate. She had moderately swollen and tender proximal interphalangeal joints. Her other joints were unaffected, but she had generalized muscle aches. The results of investigations are shown in Figure-26.

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A science teacher guides to help a student explore and understand key concepts in science such as reading research essays examples, gathering evidence to support ideas and solving problems. Science teachers are responsible for coming up with lesson plans, presenting demonstrations, and giving assignments. They identify learners who are struggling to grasp various concepts and help them achieve their goals. They also need to communicate with the school administration and parents regularly about students’ progress.

Job requirements and tasks

Science teachers are required to prepare lesson plans based on school policies and grade levels. This includes preparing outlines, class assignments, homework, special projects, and tests. Tutors need to maintain student records on grades, class attendance, and conduct according to school and state policies. They also need to evaluate student performance regularly.

You need to have excellent verbal and written skills to communicate with students, school admin, and parents. You have to be detail-oriented, have good instructional skills, and solve problems effectively. You should also be actively involved in extracurricular activities such as athletics, football, and school clubs. Having a bachelor’s or master’s degree in science and a tutoring certificate is essential if you want to teach in public schools. To teach in higher learning institutions, you need to have a doctoral degree.

Becoming a science teacher

To become a science tutor in a public learning institution, you need to have a teaching license or certificate from your country or state together with an endorsement to teach this subject. Tutors in middle and high school usually major in the subjects they want to teach such as chemistry or biology. On the other hand, teachers at the elementary level teach a wide range of subjects. For private schools, you might not require a certification since the qualifications vary. To become a secondary school teacher in a public school, you need to:

* Have a degree in the subject you want to teach and complete all the required preparations
* Complete your teaching internship in the grade level you want to teach
* Take the required tests to get state approval
* Apply for a teaching license
* Apply for teaching jobs being advertised to science teachers

If you already have a college degree but lack other requirements, don’t fret. Getting certifications from your state is easy as long as you follow the rules.

Salary and outlook of the job

The Bureau of Labor Statistics shows that science teachers at the elementary level earn an average salary of $57,980 while middle and high school teachers earn $58,600 and $60,320 respectively.

A 3 to 4 percent job growth is expected for all the groups. Science teachers who have a master’s degree earn an average salary of $82,550. The job growth prospects are at 11 percent. There are a lot of career advancement opportunities for science teachers who focus on developing and improving their skills regularly.

Getting a teaching job

To land your dream job, you’ll need to write and submit a professional resume that lists your education, job history, teaching experience, and accomplishments. Having affiliations with professional organizations that focus on science education can increase your chances of landing the job.

Start your job search by visiting school websites and other places that are dedicated to posting teaching jobs exclusively. Ensure that you have all the credentials to avoid wasting time and energy.


Trained science teachers have a lot of amazing job opportunities in the market. To increase your chances of landing a job and getting promotions, you need to develop and improve your skills regularly and network frequently. Getting the facts right and using the right procedures will help you achieve your
career goals quickly.

The Best Biological Universities In The World

Every person dreams of choosing a profession that would not only always be in demand, and therefore highly paid, but also beneficial to society. One of such prestigious professions is the profession of a biologist. Their professionalism largely determines our health, development, and future. Therefore, it is not surprising that the profession of a biologist is the second most popular in the world.

Many decent biology students dive into the practical study so much that they don’t have time for other college assignments. Some of them simply google something like “write my paper with WritingAPaper writers” in order to keep up with their academic performance and save time for more essential college practices. 

However, not everyone can get this necessary and promising profession because it puts forward several requirements that only people with particular inclinations and temperaments can meet. So, we will take a look at the features of these professions and also take a look at the top-rated biological universities in the world.

What Personality Traits Should A Biologist

It is not difficult to guess that a biologist, first of all, must love nature and be interested in the appearance and development of life on Earth. In addition, a true biologist is characterized by:

  • analytical and logical thinking;
  • curiosity and patience;
  • accuracy and attentiveness;
  • observation and imagination;
  • a well-developed visual, imaginative memory;
  • assiduity and concentration abilities;
  • responsibility and honesty.

It should be noted that since the work of a biologist involves participation in laboratory research,
which often uses various chemicals, the specialist should not tend to allergies.

Advantages of the of the Biology Profession

As mentioned above, biology is an actively developing branch of science, which opens to specialists huge prospects for career growth and self-fulfillment. Another undoubted advantage of the biology profession is the demand for it. According to labor market experts, this profession, in the coming years, may become one of the most in-demand and highly paid.

An essential advantage of this profession is a great variety of institutions and organizations where you can show your talent and professional skills. Today, biologists are happily employed in research laboratories, environmental organizations, nature reserves, botanical and ecological gardens, research institutes, environmental organizations, agricultural industries, and educational fields (schools, colleges, universities).

Disadvantages of the Biology Profession

Even though biology is one of the most in-demand fields of science in the world, in some countries, this field is still in its infancy. So, biologists’ salaries are low, primarily if they work in public institutions (for example, in laboratories at research institutes or schools).

The job of a “practicing” biologist (a specialist who studies living organisms in their natural environment) involves frequent business trips. These specialists can be found everywhere: in the desert, in the tundra, high in the mountains, in the field, and at the experimental agricultural station. Naturally, conducting research in comfortable conditions is not always possible, so future biologists must be prepared for life in spartan conditions.

More often than not, theoretical training alone is not enough for successful employment for young professionals. Therefore, biology students need to take care of practical work experience in advance (i.e., while still studying to look for a job in a specialty as close to their future profession as possible).

The best biological universities in the world

American universities are leading the way among educational institutions, but other continents also have something to show for it.

Check out lists of the strongest universities in North America, Europe, and Asia.

1. Harvard University (USA)

Harvard University is considered No. 1 in the world in genetics, genomics, and bioinformatics, as well as in biochemistry and biophysics by US News & World Report. Harvard’s biotechnology education program allows students to pursue bioengineering, nanotechnology, and bioinformatics. The Department of Molecular and Cell Biology is considered the best at Harvard. This multidisciplinary approach trains not only scientists but also people for managerial positions in the biotechnology field.

2. University of Tokyo (Japan)

The Department of Biotechnology offers graduate programs in biomolecular research, biofunctionalism, and molecular and cellular biosciences. Students study DNA, protein engineering, and bioinformatics. Importantly, master’s students take international internships.

3. University College London (UK)

University College London is regularly ranked in the top 10 of various prestigious rankings of the best biotechnology universities. Students receive their first higher education in biochemistry (studying chemistry, biochemistry, genetics, and molecular biotechnology). The master’s degree in biotechnology specializes in critical areas like cell regulation, molecular cloning, and others. The most crucial area of study here is experimental biochemistry.

4. University of California San Francisco (USA)

The university offers some of the world’s best programs in biochemistry and biophysics, the fields closest to biotechnology. Molecular biotechnology programs and internships are by far the most popular. Graduate students have the opportunity to combine scientific research with professional business experience, allowing them to quickly find work after graduation in the rapidly growing biotechnology sector.

5. University of Pennsylvania (USA)

The university offers bachelor’s, master’s, and Ph.D. programs in biotechnology and a so-called “professional master’s degree” in biotechnology. Students can choose a major in molecular biotechnology, biopharmaceuticals/engineered biotechnology, or biomedical technology. A dual degree with Wharton University is also available.

6. Massachusetts Institute of Technology (USA)

Founded in 1998, the Department of Biological Engineering quickly became one of the best in the world – it couldn’t be otherwise at the best technological university on the planet (according to the latest rankings). It has first-class laboratory facilities in biomedical engineering, environmental and health sciences, microbiology, etc.

7. Johns Hopkins University (USA)

You are offered with undergraduate and graduate programs in biotechnology by The Center for Biotechnology Education at Johns Hopkins University. Students receive core knowledge in biochemistry, molecular biology, cell biology, genomics, and proteomics. Students also study applied science and the application of new technologies to business, as well as opportunities for overseas internships. There are also part-time and distance learning programs.

8. Rensselaer Polytechnic Institute (USA)

Rensselaer Polytechnic Institute was founded in 1824 and is considered to be the oldest technological university in the United States. The Center for Biotechnology and Interdisciplinary Sciences offers a number of programs, including a top-rated program at the interface between biotechnology and medicine.

9. Stanford University (USA)

Stanford University, one of the top universities in the world, offers an excellent program in the Department of Bioengineering. The program was jointly developed with the Department of Medicine and Engineering and focuses on engineering approaches to medical problems and biological systems. The university also offers tempting internship opportunities at leading companies in the industry.

10. University of Rhode Island (USA)

This renowned university offers several undergraduate and graduate-level biotechnology programs. Much research focuses on stem cell biotechnology, molecular biotechnology, and bioprocesses.

We hope you will easily get accepted to one of these universities and make your dream of becoming a successful biologist come true.

12 Compelling Reasons Why Studying Biology Is the Right Choice for You

If you are pondering whether you should start a biology major or maybe you’re pondering whether to continue because it’s not what you expected, this post is addressed to you. And I hope that after reading it, the answer to both questions is a resounding YES!

Studying Biology

Let’s begin!

1. It’s your calling

If you think it is, then don’t hesitate to act on it! Do you want to buy a college essay or other papers all the time because you are disinterested in your major? Nothing is as satisfying as dedicating yourself to what you are passionate about. Nothing. So don’t miss this opportunity. I’ve always said I’d rather be poor but happy with what I do than rotten with money and bitter at my desk. Don’t miss this chance to achieve personal and professional happiness by doing what you love most. 

2. It changes the way you look at everything

Being a biologist is a way of life. It is the lens through which you end up filtering everything around you. Studying biology will change you on a very deep level, and you will learn to see the world through different eyes. And trust me, it’s an experience worth having. 

3. Biology has opportunities

You can work in more than just science, as a teacher, or as a government employee. There are many career options, and some are waiting for you to discover them. It only takes courage and imagination. Working for one of the best essay writing services, you can also help students with their biology assignments. Opportunities are waiting for you to discover them.

4. You contribute your grain of sand to universal knowledge

Like all sciences, it opens up the possibility of becoming part of a trove of knowledge that humanity has been collecting since time immemorial. It is unlikely (though possible) that you will make a remarkable discovery, but you will certainly contribute to the building of knowledge, either by adding a brick or by getting more people to visit it: scientists, teachers, disseminators, environmental educators… 

They all contribute to the dissemination of this knowledge. Even conversations between colleagues over a few beers can get someone else to come and learn a little more about this amazing world we live in.

5. Great travel opportunities

Few professions require such high mobility, both voluntary as part of your studies and mandatory as you have to emigrate to other countries to make a living. With all the consequences that entail. All the great travelers I have met have a powerful aura around them, a powerful magnetism. Their outlook on life, their understanding of it, and their attitude toward other people and the world are imbued with all the experiences gained during their travels. Wouldn’t you like to be one of them? 

6. It’s fascinating

In biology, it doesn’t matter what you study, it doesn’t matter what you work on. Whatever you do, you will enjoy it. Of course, it’s not a bed of roses; it requires a lot of sacrifices and some struggle. But if you finally find your way and follow it, I assure you, you will live it intensely (for better or for worse). Many biologists I know, even if they don’t work in biology, retain the passion and connection to nature and life that they acquired during their studies.

7. It is a journey of discovery

And by that, I don’t just mean scientific discoveries, but personal ones as well. This is a very challenging career and profession. Unless you are one of those rare and genius geniuses who show up from time to time, you will have to constantly put your best foot forward. 

It will force you to explore your limits and get to know yourself better. But you will also discover new areas of knowledge that you thought you would never be interested in. You will learn a lot about yourself, I guarantee it.

8. It’s a lot of fun

Biologists have a very specific idiosyncrasy. No matter what country or field you work in, there are always some common traits that are common to almost all of us (although there are exceptions). I can tell you that the best parties I’ve been to have always had biologists in attendance.

I don’t know what things are like at your university, but while I was studying, when I was getting my degree, whenever a lot of biologists gathered, it always ended with a few beers: with people from your science group, after a paper, after a conference, on a field trip… And I can assure you that I was with people of all ages and from all walks of life.

9. You will meet many people

As with any career, you will say. However, ours has many features that make networking in biology something fundamental. Much of the work you will do during and after your degree will have to be done in the company of other people. Collaboration is fundamental in the biological sciences: articles, conferences, research, or conservation projects… You always need a team. So try to choose the best.

10. You will discover wonderful spots you never saw before

Once you begin to familiarize yourself with the flora and fauna and begin to visually identify species without the help of guides, a whole new world opens up before you. It is when you walk down the street of your town or village that a whole new life unfolds before you. 

Where you once thought there were only house sparrows (Passer domesticus) or loons (Diplotaxis virgata), now a whole plethora of living creatures unfolds that previously went unnoticed before your astonished eyes. Then you learn about the little living paradises, those islands of nature amid civilization, which surround you and are waiting for you to find them.

11. It’s an adventure

As you may have heard. The job of a biologist is one of the most adventurous professions, in the most romantic sense of the word. Remote and inhospitable places, which can range from the most enclosed jungle to the icy expanses of Antarctica. Challenging situations, sometimes not without risk, to get the data you need. Adrenaline, discovery, excitement. If you really want it, you can try a little bit of all of them.

12. Direct contact with nature

What better way to be one with nature than to work as a biologist? You can work with the kinds of animals you like, from the most common to the most exotic. Plants or animals-you choose the path. Or even those creatures that straddle the blurry line between living and non-living, such as viruses or prions. From the largest to the smallest. From your lab or deep in the woods. To study life, you have to go where it is. What other contact can you ask for?

Final words

If it is not yet clear to you, perhaps this career is not for you. But if reading any of these reasons made you feel identified, making your heart beat faster, or made you smile, then don’t hesitate and act. Because biology must be lived, and how else can you study life?

Proper Lab Report Format You Need to Know to Pass with Flying Colors

Learning how to construct a proper lab report will not only secure you with a stellar grade in your science class, but it also will teach you how to report coherently your scientific findings to the world once you are in the field. Lab reports are an essential part of the scientific process and are constructed always after a scientific experiment or study. Therefore, learning the proper lab report format is integral to your overall success.

Below, we have detailed all the components of your lab report and have explained the elements that must be included in your rough draft. If you adhere to our guidelines, you will have all the pertinent information you need to get yourself that A on your lab report.

How to Draft Your Lab Report

This goes without saying, but you need to have a thorough grasp of the material that you are studying before you can write your report. If there are elements you are unsure about and that need clarification, make certain you get that missing information before you write your report.

Your lab report needs to show that you have a complete understanding of the experiment or study you are covering, but it can sometimes be difficult to keep track of all the information you have covered in your experiment. To keep yourself organized, make a rough draft of your report with the following points in mind.

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Questions You Need to Answer before Starting Your Report

To make things easier for yourself, you need a clear outline that provides answers to specific questions the report will be answering. Jot down the answers to the following questions before writing your lab report to help you cohesively tie together all the information in your experiment:

  • What do you hope to learn from the experiment?
  • What is the hypothesis you are testing?
  • What will be done in the experiment?
  • Why is this method the best way to test your hypothesis?
  • Why would the scientific community (or classroom) benefit from the knowledge presented in the experiment?

Answering these questions will put you in an excellent position to draft an impressive lab report and give you a thorough understanding of the material at hand.

Double Check Your Data with Your Lab Partners

Human error is likely to happen from time to time, and nothing is more important in your lab report than the accuracy of your data. To ensure you and your lab partners are on the same page and that you all have the correct data, get together after you have completed your experiment to double check your findings. It is much better for you to catch this mistake now than for your professor to catch it while grading your report and deduct points for the error.

Know How to Use APA Format

Before you begin your lab report, it is important that you know the basics. APA format is the most widely used format for lab reports and has specific guidelines that you need to follow. Make sure that your paper is formatted properly so that you get the highest grade possible. Nothing is worse than writing an amazing report only to have your professor deduct points for improper formatting.

The following should be consistent throughout your entire report to reflect proper APA formatting:

  • Paper is double-spaced
  • Margins are one inch all around
  • Font is 12 point Times New Roman
  • Manuscript page header with page number appears in the upper right-hand corner of every page

Write with Your Audience in Mind

Finally, before you write your lab report, make sure you know the audience to whom you are addressing. Write the report as if you are explaining it to a clueless student to ensure that you are thorough and accurate in your reporting. Addressing your report solely to your professor may cause you to gloss over simpler concepts or ideas, and this may result in a lower grade.

Proper Lab Report Format

Now that you are ready to write your report, it is important to know the proper lab report format you will be required to follow. All lab reports follow the same basic formula and comprise five sections: the title page, introduction, methods and procedure, results and discussion. These elements need to be included in your final lab report to explain thoroughly the results and findings of your scientific experiment or study.

Not only will this lab report format help to get you a good grade in class, but it also will get you accustomed to the professional standard that will be expected of you once you are in the field. Below, you will find detailed descriptions of each section, as well as the main points you need to cover in each section.

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Section One: Title Page

First things first. Proper lab report format calls for a title page that describes in 10 words or less what your scientific experiment is proving. Titles should start with an action word and vividly describe the premise of the experiment. A successful title will describe succinctly the main idea behind your experiment or study and entice the reader to learn more about your research. The title page also should include your name and your lab partner’s name, your instructor’s name, and the date on which the report was submitted.

Section Two: Introduction

Proper lab report format always will include a thorough introduction of about 150-200 words that includes four basic elements: the purpose of the experiment, the tested hypothesis, a reasonable justification of your hypothesis and a stated connection between the experiment and relevant background research/information.

An easy way to structure your introduction would be to start by first stating your purpose. From there, it is easy to segway seamlessly from your purpose to the relevant background information (often taken from class learnings or lectures) supporting your purpose. This will lead you to the conclusion of your introduction. Here, you will state your hypothesis and reasonable justification of that hypothesis in the final sentences.

This wording method for your introduction is common, but unnecessary. Feel free to experiment with different sentence structures that better suit your particular subject matter, if applicable.

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Section Three: Methods and Procedure

The goal of this particular section is to describe in succinct detail how you tested your hypothesis as well as to provide a reasonable justification and rationale for your chosen procedure. Remember that the goal of scientific research is for it to be reproducible; therefore, other researchers should be able to follow your procedure so they can verify your findings through the same or similar collections of data. For this reason, aclearly defined method and procedure are of the utmost importance to creating a successful lab report.

To begin this section, it is best to list all the materials you used in your method and procedure, as well as to define explicitly the control variable in the experiment. The best way to structure this section is to keep it simple and just follow the chronological narrative that occurred as you were conducting your experiment. Be detailed and always explain the rationale behind what you are doing to show an expert understanding of the material.

Make sure that you are being specific and detailed about how you got your results. Explain thoroughly what you are doing and why you are doing it. Also, be sure to explain what you plan to do with your findings. Quantify all measurements such as time, temperature, volume, mass, etcetera to maintain accuracy throughout this section. You may briefly mention how you quantified and recorded your results and data, but be careful not to jump too far ahead and describe the results in too much detail.

You may want to considering separating the material into subheadings corresponding to each individual component in this section if you had a particularly long or involved experiment to ensure clarity for the reader. However, this is not a standard lab report format and it should only be used if you have a long list of materials to document or if your procedure was convoluted.

It also is important to remember to use proper grammar in this section to avoid any confusion. A common mistake is to use the present tense for describing your experimental procedures because you are writing it in the present tense. However, you must use past tense to described the experiment that occurred in the past to avoid any uncertainty.

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Section Four: Results

The results section is the backbone of your lab report; all other sections of the report depend entirely upon the existence of this section. This is perhaps the most self-explanatory section included in your lab report and may even be your shortest. The goal of this section is to document and highlight all the data that is significant to your hypothesis. You do not need to list every piece of data you have collected because not all the data will be relevant.

All you need to focus on here is to report the data that either proves or disproves your hypothesis in the form of three distinct parts: text, tables and figures. All results sections will start with a brief text description that clearly states the facts of the data. However, be sure not to add so much text that it becomes analytical; you can save that for the next section. In your brief text descriptions, you will want to point out what your data shows in your tables and figures. You may also want to acknowledge and state trends that arise in your data.

Next, you will want to include your tables that show the trends in your data. As a general rule, you will only want to use tables if you have any variation in your data. If you have relatively unchanging variables, a table will not be the effective medium to display your data. You also will want to be sure to give your table a relevant name and have the reader see the data vertically rather than horizontally.

Finally, you will conclude your results section by showing your readers a figure that demonstrates what happened to your independent and dependent variables as you carried out your experiment. Depending upon the subject matter, you can include pie charts, bar graphs, flow charts, maps or photographs in this section. Do note, however, that proper lab report format for undergraduates and industry professionals will be a line graph.

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Section Five: Discussion

Finally, to conclude your lab report you will need to detail your findings and determine whether your hypothesis was supported by your experiment. There are five goals that need to be accomplished with this section, which include:

  • Explaining whether the data proved your hypothesis
  • Mentioning and interpreting any data that deviated from what you expected
  • Detailing reasonable conclusions about the subject matter that you studied
  • If applicable, relating your research to earlier work in the same field
  • Discussing the practical and theoretical implications of your findings

Most discussion sections will begin with explaining how your data either supported or denied your hypothesis. From there, you will need to make explicit statements that explain how your experiment either supported or denied your hypothesis. Your lab report should be able to support a reasonable and justifiable claim based upon the results of your experiments, so be sure that you are very clear and concise in your wording here.

It is important to note that this section will have the most variability from a standard lab report format. It should be tailored to your specific subject matter and subsequent results as long as it meets the above requirements and goals.

Putting It All Together

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Writing out a lab report can be the most difficult part of any experiment, but now that you know the proper steps and format you will be able to earn that A+ you deserve. Due remember to always follow the proper lab report format that we outlined above and you will be passing all of your science classes with flying colors.

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