title: [The role of regulatory cells CD4+CD25+ in the development of chronic infective diseases].
abstract: Regulatory T-cells CD4+CD25+Foxp3 (Treg) present a small subpopulation of CD4+ T lymphocytes, which develop in the thymus and are disseminated into peripheral lymphoid organs on the 3rd or the 4th day of the neonatal period. Treg play a decisive role in the pathogenesis of autoimmune diseases and the development of tolerance to transplantation antigens, regulate the immune response to allergens, and suppress antimicrobial immunity. Treg suppress proliferation as well as the cytotoxic effect and the secretion of Th1 and Th2 cytokines by effectory T lymphocytes, thus limiting the strength of the immune response of effectory T-cells, which makes them impossible to adequately control viral and bacterial infections. Recognition via antigen-presenting cells and the subsequent induction of the proliferation of antigen-reactive T and B lymphocytes, directed towards infectious agent elimination, is accompanied by the activation of regulatory T cells as well, which leads to immune response suppression; repeated microbial infections are not only able to strengthen T-cell immunity by generating memory T-cells, but can also strengthen the suppressive activity of endogenous T regulators CD4+CD25+. Moreover, T reg are capable of the direct recognition of a microbial product; these cells selectively express Toll-like receptors (TLR)-2, -4, -5, -7, and -8. Under normal conditions T reg are anergic, but are capable of direct proliferation in response to stimulation by TLR ligands, expressed on microbes and parasites. Treg removal enforces protective immune response to contagious microorganisms, including bacteria, viruses, and fungi, which leads to the elimination of pathogens from the host organism. The removal of Treg population will help to accomplish infectious pathogen elimination and diminish inflammation within a short period of time.
authors.forename: A A
authors.initials: AA
authors.lastname: Vorob'ev
authors.forename: S N
authors.initials: SN
authors.lastname: Bykovskaia
authors.forename: E P
authors.initials: EP
authors.lastname: Pashkov
authors.forename: A S
authors.initials: AS
authors.lastname: Bykov
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D002478:Cells, Cultured; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D015658:HIV Infections / Q000276:immunology; D006801:Humans; D007156:Immunologic Memory; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology; D008024:Ligands; D008213:Lymphocyte Activation; D051379:Mice; D009181:Mycoses / Q000276:immunology*; D010272:Parasitic Diseases / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology; D014777:Virus Diseases / Q000276:immunology*
chemical_list: D016207:Cytokines; D053645:Interleukin-2 Receptor alpha Subunit; D008024:Ligands; D051193:Toll-Like Receptors