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Disturbances in immune tolerance provoke autoimmune aggression, i.e., a specific immune response to auto-Ags with subsequent development of an autoimmune syndrome or an autoimmune disease (Suchkov et al., 2007). A crucial role in formation of autoimmune syndromes and progression of autoimmune diseases is played by inborn (in the first place, HLA-associated) predisposition coupled with impaired immune responsiveness of the invaded organism. Noteworthy, initiation and progression of autoaggressive reactions cannot be triggered without preliminary activation of signaling reaction cascades, which include: i. polyclonal activation of autoreactive cytotoxic T lymphocytes (CTL) by super-Ag (multimolecular protein complexes composed of microbial Ags, Ags and/or haptens of the carrier or intermediary drug-related metabolites) demonstrating broad spectrum of epitopes; ii. release of sequestered or intramolecular (cryptic) autoepitopes after the tissue damage or organ injures during the inflammatory process; iii. anti-idiotypic Ab formation that can damage own tissue and promote autoagression; iv. effect of mimicking epitopes (microbial Ags cross-reacting with autoepitopes of human tissues and organs). Of particular interest in this respect is so-called molecular mimicry. Its biological mechanism is based on cross-reactivity, i.e., ability of the infected organism to cross-react, by virtue of structural homology between its auto-Ags and microbial Ags, with the microbial antigen thereby triggering miscellaneous immune reactions. Under these conditions, the role of autoaggressors is played simultaneously by two different groups of Ags, namely, mimicking Ags of the microbial pathogen and patient’s own autoAgs. Their interactions form the clinical picture of the postinfectious autoimmune syndrome (PIFA), one of main clinical variants of syndromeal immune pathology (Paltsev et al., 2009a). Today, the key role of the immune system in the pathogenesis of chronically relapsing infectious diseases (CRID) leaves no doubt. Their clinical course is controlled by an immense variety of factors and their combinations among which the immunologic syndrome (IS) reflecting the origin and severity of disturbances in immune homeostasis occupies a special niche. The concept of IS is not new in principle and is widely met in the current literature.

Postinfectious Autoimmune Syndrome as a Key Factor in Chronization of the Infectious Disease