MOLECULAR MIMICRY
MOLECULAR MIMICRY
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DOI：
10.1016/b978-044452763-9/50007-x
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发表时间：
2007-01-01
期刊：
影响因子：
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通讯作者：
Fujinami, Robert S.
中科院分区：
文献类型：
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作者：
Peterson, Lisa K.;Fujinami, Robert S.
Molecular mimicry is the occurrence of common B or T cell reactive epitopes between microorganisms or environmental agents and the host, and the pathogenic consequence of such cross-reactivity. Molecular mimicry has been demonstrated to occur in several different forms including complete identity at the protein level, homology at the protein level, similarity at the level of amino acid sequences and structural similarity. Identification of cases of molecular mimicry as a cause of autoimmunity can aid in the prevention, prognosis and treatment of patients with autoimmune disease. For the conclusion that molecular mimicry causes autoimmune disease, several criteria must be fulfilled: (1) similarity between a host epitope and an epitope in a microorganism or environmental agent, (2) antibodies or T cells cross-reactive with both epitopes detected in patients with the autoimmune disease, (3) an epidemiological link between exposure to the environmental agent or microbe and the development of autoimmune disease and (4) reproducibility of autoimmunity in an animal model following sensitization with the epitopes, infection with the microbe or exposure to the environmental agent. Few proposed molecular mimics have been shown to fulfill all these criteria. However, Campylobacter jejuni lipooligosaccharide (LOS) mimicry of human GM1 ganglioside and mimicry between the dietary antigen butyrophilin and myelin oligodendrocyte glycoprotein provide examples that fulfill all the criteria, thus providing support for molecular mimicry as a viable mechanism for the development of autoimmune disease.
