[The significance of regulatory CD4+CD25+ T cells in the pathogenesis and treatment of kidney disease].
Thanks to a precisely regulated response, the immune system works to maintain homeostasis, and one of the significant mechanisms of this regulation is regulatory T cells. This paper presents the latest knowledge concerning the occurrence of natural regulatory T cells of CD4+CD25+ phenotype and their role in the pathogeneses of immune system diseases. Functional and quantitative disorders in this population of cells are found in many diseases which in their course attack the kidney, for instance mixed cryoglobulinemia, rheumatoid arthritis, Sjögren's syndrome, lupus erythematosus, and type 1 diabetes mellitus. The role of T cells and the effectory and regulatory mechanisms dependent on them in the development and progression of glomerulonephritis is presented. The role of regulatory T cells in the development and progression of chronic kidney disease is discussed as well. Qualms whether a decreased number and/or disrupted function of regulatory T cells promote the development of autoimmune diseases or whether they are secondary phenomena are settled by clinical observations in which restoration of the number of the cells prevents further tissue damage. Strengthening or blocking regulatory T-cell functions and obtaining a balance between activation and suppression in the immune system depending on current needs may become the key to the immunotherapy of many diseases. Another problem presented in this paper is the perspective of regulatory T cell therapy; however, attempts to modify their activity and change the number of cells must be carried with the greatest of care because such a procedure may result in dysregulation of the immune system.
Krajewska
Magdalena
M
Klinika Nefrologii i Medycyny Transplantacyjnej Akademii Medycznej we Wrocławiu, Poland. magda@softstar.pl <magda@softstar.pl>
Weyde
Wacław
W
Klinger
Marian
M
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology; D001323:Autoantibodies / Q000276:immunology; D015551:Autoimmunity / Q000276:immunology; D015704:CD4 Antigens / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000145:classification / Q000276:immunology*; D004195:Disease Models, Animal; D005921:Glomerulonephritis / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D007167:Immunotherapy / Q000639:trends; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D051436:Renal Insufficiency, Chronic / Q000276:immunology / Q000503:physiopathology; D012859:Sjogren's Syndrome / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000473:pathology
D001323:Autoantibodies; D015704:CD4 Antigens; D053645:Interleukin-2 Receptor alpha Subunit