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• W1444398617 abstract "Systemic lupus erythematosus (SLE) is an autoimmune disorder that is complex in clinical manifestation and, most likely, in etiology. This chapter focuses on molecular mimicry of host structures by microbial pathogens, one of the possible mechanisms that contributes to autoreactivity in lupus. Studies of serum from patients with bacterial infections led to the realization that nonautoimmune hosts, during the time of infection, make antibodies with specificities similar to those of autoantibodies in sera from patients with SLE. Reciprocal inhibition assays with dsDNA and pneumococcal polysaccharide performed with three of the cross-reactive antibodies demonstrated that dsDNA and polysaccharide bind at the same or a proximal site on these antibodies. DNA-protein binding usually requires a more polar interface and a far greater number of hydrogen bonds, both direct and water mediated, than protein-protein interactions. The anti-DNA specificity is generated both by activation of cross-reactive antibodies and by the process of somatic mutation but is most likely downregulated by the normal host. The cross-reactivity may be germ line gene encoded or may be generated by somatic mutation of the antibody. Nonautoimmune hosts can generate B cells with potentially pathogenic autospecificities, and the antigenic relatedness of DNA to carbohydrate antigens is sufficient to activate cross-reactive B cells. In humans, it remains to be determined if this cross-reactivity is potentially pathogenic; in mice, it clearly is. Immunization with a peptide mimotope of DNA can also induce lupus-like autoreactivity in mice." @default.
• W1444398617 created "2016-06-24" @default.
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• W1444398617 date "2014-04-08" @default.
• W1444398617 modified "2023-10-01" @default.
• W1444398617 title "Mimicry between DNA, Carbohydrates, and Peptides: Implications in Systemic Lupus Erythematosus" @default.
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• W1444398617 doi "https://doi.org/10.1128/9781555818074.ch10" @default.
• W1444398617 hasPublicationYear "2014" @default.
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