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The high percentage of disease-discordant pairs of monozygotic twins demonstrates the central role of environmental factors in the etiology of autoimmune diseases. Efforts were first focused on the search for triggering factors. The study of animal models has clearly shown that infections may trigger autoimmune diseases, as in the case of Coxsackie B4 virus in type I diabetes and the encephalomyocarditis virus in autoimmune myositis, two models in which viruses are thought to act by increasing immunogenicity of autoantigens secondary to local inflammation. The induction of a Guillain-Barre syndrome in rabbits after immunization with a peptide derived from Campylobacter jejuni is explained by mimicry between C. jejuni antigens and peripheral nerve axonal antigens.

Other models involve chemical modification of autoantigens, as in the case of iodine-induced autoimmune thyroiditis. These mechanisms have so far only limited clinical counterparts (rheumatic fever, Guillain-Barre syndrome and drug-induced lupus or myasthenia gravis) but one may assume that unknown viruses may be at the origin of a number of chronic autoimmune diseases, such as type I diabetes and multiple sclerosis) as illustrated by the convergent data incriminating IFN-alpha in the pathophysiology of type I diabetes and systemic lupus erythematosus. Perhaps the difficulties met in identifying the etiologic viruses are due to the long lag time between the initial causal infection and onset of clinical disease. More surprisingly, infections may also protect from autoimmune diseases. Western countries are being confronted with a disturbing increase in the incidence of most immune disorders, including autoimmune and allergic diseases, inflammatory bowel diseases, and some lymphocyte malignancies. Converging epidemiological evidence indicates that this increase is linked to improvement of the socio-economic level of these countries, posing the question of the causal relationship and more precisely the nature of the link. Epidemiological and clinical data support the hygiene hypothesis according to which the decrease of infections observed over the last three decades is the main cause of the incessant increase in immune disorders. The hypothesis does not exclude an etiological role for specific pathogens in a given immune disorder as might notably be the case in bowel diseases. Even in this setting, infections could still have a non-specific protective role. Independently of the need for confirmation by epidemiological prospective studies, the hygiene hypothesis still poses numerous questions concerning the nature of protective infectious agents, the timing of their involvement with regard to the natural history of immune diseases and, most importantly, the mechanisms of protection. Four orders of mechanisms are being explored. Antigenic competition is the first hypothesis (immune responses against pathogens compete with autoimmune and allergic responses). This is probably an important mechanism but its modalities are still elusive in spite of considerable experimental data. Its discussion in the context of homeostatic regulation of lymphocyte pools has shed new light on this hypothesis with possible competition for self MHC peptide recognition and interleukin-7. Another hypothesis deals with immunoregulation. Infectious agents stimulate a large variety of regulatory cells (Th2, CD25+, Tr1, NKT, ...) whose effects extend to other specificities than those which triggered their differentiation (bystander suppression). Infectious agents may also intervene through components which are not recognized as antigens but bind to specific receptors on cells of the immune system. Major attention has recently been drawn to Toll receptors (expressed on macrophages and possibly on regulatory T cells) and TIM proteins present on Th cells, which may express the function of the virus receptor (as in the case of the Hepatitis A virus and Tim-1). Experimental data will be presented to support each of these hypotheses. In any event, the final proof of principle will be derived from therapeutic trials where the immune disorders in question will be prevented or better cured by products derived from protective infectious agents. Numerous experimental data are already available in several models. Preliminary results have also been reported in atopic dermatitis using bacterial extracts and probiotics.


Geneticists have identified a link between the number of copies of a specific gene an individual has and their susceptibility to autoimmune diseases like lupus. Research using DNA has revealed that people who have a below average number of copies of a gene, known as FCGR3B, have an increased risk of developing diseases caused when the bodys immune system attacks its own tissue.

The research by Professor Tim Aitman of the Medical Research Council Clinical Sciences Centre at Imperial College London, and colleagues, is published in Nature Genetics.

Professor Aitman explains the teams research discovery:

The variations in DNA that people carry contribute to observable characteristics like height, weight and skin colour. Genetic variations have similar effects on individual susceptibility to disease. In this research our team focused on structural differences in the genome and set out to determine whether the number of copies of a particular gene a person has influences their chances of developing an autoimmune disease. We discovered that not only does the number of copies of a gene you have influence your chances of disease but that this kind of structural variation in the genome could be driving evolution of human weaknesses for infection and inflammation. The team studied DNA from two groups of people living in the UK and France. They discovered that people who have a comparatively low number of FCGR3B genes are more likely to suffer from autoimmune diseases like lupus (systemic lupus erythematosus) that affect the whole body. The same link was not found to autoimmune conditions affecting just one organ such as Addisons disease, which damages the adrenal gland, or Graves disease, which attacks the thyroid.

Human genome research increasingly provides evidence that individuals vary in the number of copies of genes present in each of their genomes. Professor Aitman concludes:

Our discovery highlights the importance of gene copy number variation, that is differences in the number of copies of a specific gene a person carries, in genetic predisposition to common human diseases. The next step is to find out whether genes that are closely related to this susceptibility gene, FCGR3B, also vary in copy number and predispose to similar diseases.

The research team hopes to achieve these aims by studying the genomes of individual people to find out if there is any correlation between gene copy number and patterns of disease presentation or responses to specific treatments.


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