The studies summarized in this chapter indicate that chronic bacterial, viral, and parasitic infections can serve as a trigger factor of autoimmune reactivity according to various mechanisms. The relationship between microbes and autoimmunity could be manifested by the presence of autoantibodies, autoimmune complexes, or T cells with autoactivity. The presence of autoimmune phenomena in chronic infections could be related to polyclonal B-cell activation, molecular mimicry between microbial and host antigens, altered self, abnormal expression of immunoregulatory molecules, and the anti-idiotypic network. In most cases, the appearance of self-reactivity in the sera of patients with chronic infections is not associated with clinical manifestations. These findings suggest that autoimmune disease is the result of a combination of factors including immunologic, genetic, hormonal, and environmental. Infectious agents have a role in the breakdown of tolerance and the appearance of autoreactivity. However, only patients with the proper immunogenetic and hormonal background may develop clinical manifestations of autoimmune disease. In spite of the extensive knowledge that has accumulated, the specific relationship between infections and autoimmunity is still obscure. Clearly, additional studies are required to clarify the relevance of microbes to the pathogenesis of autoimmune diseases.
|Number of pages
|Published - 1 Jan 1991