Autoimmune diseases infectious agents

Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown aetiology with some autoimmune features. Current thinking favours the hypothesis that interplay between genetic factors, sex hormones, and possibly an infectious agent or another immune activating agent initiates an autoimmune pathogenic mechanism that culminates in a disease with inflammatory and destructive features. 

There is considerable interest in the role of infectious agents in the development of autoimmune diseases. Some of this interest is based on the concept of molecular mimicry as a causal mechanism. Molecular mimicry refers to the possible pathologic role of cross-reactive antibodies or T cells to a self-antigen that is structurally similar to, and thus shares epitopes with, a viral or other infectious agent. For most autoimmune diseases, however, evidence of molecular mimicry leading to disease is not conclusive.1819 Viruses and other infections also have a less-specific immune effect, stimulating toll-like receptors and proinflammatory cytokine secretion, which is another mechanism that has been postulated to influence autoimmune disease risk.20... 

This chapter reviewed current research pertaining to selected environmental agents and autoimmune diseases (Table 25.3). Other infectious agents (e.g., parvovirus, varicella), occupational exposures (e.g., mercury), dietary factors (dietary supplements, nutrients such as antioxidants, and specific proteins in wheat and other grains implicated in celiac disease), and stress have been the focus of additional research that was not included in this review. 

Strong mechanistic evidence from rodent models of autoimmune disease of viral or other infectious agents affecting autoimmunity or progression to overt disease, but harder to demonstrate in humans. Enterovirus (Coxsackie virus) focus of epidemiologic studies in type 1 diabetes, Epstein-Barr virus focus of epidemiologic studies in multiple sclerosis and systemic lupus erythematosus. 

To respond to the criticism of an increased prevalence of both autoimmune and allergic disease, an alternative mechanism has been proposed. According to this hypothesis, a lack of stimuli from infectious agents during development results in poor development of T regulatory cells. A poor T regulatory cell function increases the risk of the development of an autoimmune response due to the inability to suppress THi function, which may also lead to an enhanced TH2 response. 

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