Antibody molecular mimicry

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... 

Taken together, these results suggest that molecular recognition of the dodecapeptide by antibodies differs from its recognition by concanavahn A, and that the immunological cross-reactivity observed in some studies does not reflect structural mimicry. That molecular recognition by concanavalin A of carbohydrates and peptides differs has also been shown in structural studies. Here, the functional molecular mimicry observed with respect to different receptors should not be assumed to imply structural mimicry—the inter-molecular interactions may differ in each case. 

Volume 178. Antibodies, Antigens, and Molecular Mimicry Edited by John J. Langone... 

Antigens with molecular mimicry. There is also evidence that antibodies induced by viruses or bacteria can cross-react with autoantigens. 

Current opinions on cause and mechanism include the possibility that MS is often due to a form of molecular mimicry, in which an immune response to an infective or other exogenous agent leads to the formation of antibodies and/or cells that cross-react destructively with components of normal myelin. Molecular mimicry is well established in certain other disorders of the nervous system (Candler et al., 2006) including paraneoplastic syndromes (Posner, 2003). 

Keywords Acute flaccid paralysis Anti-ganglioside antibodies Campylobacter jejuni Experimental allergic/autoimmune neurids (BAN) Gangliosides Immune neuropathies Molecular mimicry T-cells... 

Figure 20.4. Glycan structures (mimics) expressed by different microbes tliat are invoked in molecular mimicry. Tlie term like is used when glycan structure has been determined by biochonical/mass spectrometry studies and term crossi eactive is used when evidence for glycan structure is indirect and based on antibody inliibition or binding studies.

Oomes PG, Jacobs BC, Hazenberg MPH, Banffer JRJ, van der Meche FGA (1995) Anti-GMl IgG antibodies and Campylobacter jejuni bacteria in Guillain-Baire syndrome Evidence of molecular mimicry. Ann Neurol 38 170—175. 

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