Molecular mimicry: its evolution from concept to mechanism as a cause of autoimmune diseases.
On a clonal level, certain antibodies and T cells can interact with dissimilar antigens found in microbes and in host cells. More than 5% of over 800 monoclonal antibodies derived from multiple RNA and DNA viruses, as well as from a large number of T cell clones, engage in such interactions. Several of these cross-reactions, which we termed molecular mimicry, are against unique host proteins involved in autoimmune responses and diseases. Thus, molecular mimicry initiated as a host response to a virus or a microbial infection, but alternatively cross-reacting with an appropriate host-antigen, can be a mechanism for instigating an autoimmune disease. Molecular mimicry provides an explanation for the genetic observation that identical twins rarely manifest the same autoimmune disease and the documented epidemiologic evidence that microbial and/or viral infections often precede autoimmune disorders.
The Scripps Research Institute , Department of Immunology and Microbial Science, La Jolla, California.
Michael B A
MB
Oldstone
D000911:Antibodies, Monoclonal / Q000276:immunology* / Q000378:metabolism; D000941:Antigens / Q000276:immunology* / Q000378:metabolism; D001327:Autoimmune Diseases / Q000276:immunology*; D006801:Humans; D007239:Infections / Q000276:immunology* / Q000382:microbiology / Q000821:virology; D018716:Molecular Mimicry / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
D000911:Antibodies, Monoclonal; D000941:Antigens