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Sergey Suchkov

Sergey Suchkov

I.M.Sechenov First Moscow State Medical University, A.I.Evdokimov Moscow State Medical & Dental University, Russia

Title: Post-infectious autoimmune syndrome (PIFAS) as an integrated and combinatorial biomarker to monitor autoimmune myocarditis and thus the chronification of post-infectious diseases of autoimmune origin

Biography

Biography: Sergey Suchkov

Abstract

Development of PIFAS as a post-infectious autoimmune syndrome (PIFAS) to illustrate a new combinatorial and integrated biomarker of the immune-mediated (including latent) disorders is featured with a progression of chronic relapsing diseases of post-infectious origin. We have investigated the syndrome-like immunopathology as applicable to chronic inflammatory processes including chronic myocarditis. In view of the structural homology immune response caused by a microbial pathogen to balance between two categories of epitopes (self-epitopes and microbial epitopes) is being developed through both autoreactive T-cells and auto-Abs. The identification of such pathogen is restricted by some difficulties. Thus, for autoimmune myocarditis (AIM) to make a bridging link with the infection is established for two-thirds of all patients, and transformation of primary (infectious) phase into PIFAS is initiated by mimicking epitopes of, for instance, Coxsackievirus (CVB3) and/or Herpesviridae (CMV), herewith presence of cardiomyosine autoreactive CTLs (CM-autoreactive CTLs) and anti-CM auto-Abs, damaging myocardium to release sequestered autoAgs and to facilitate the induction and/or development of PIFAS is required. We can stress that a tandem of two mutually mimicking epitopes (microbial and self-epitopes) is implicated in the pathogenesis of PIFAS. The therapeutic strategy for such patients should be different. And the identification of the primary pathogen or microbial associate is no less important part of the protocol being used, for what we applied immunodiagnostic screening combined with molecular diagnostics. There are no obvious clinical and laboratory criteria to get the syndrome validated. An application of transgenic models to suit the aims of clinical practice will give an opportunity to reveal the events gapped between induction and progressing of PIFAS and will allow to pre-select specific targets to control induction and progression of PIFAS and thus chronification of the clinical illness to prevent the latter in time.