Control of autoimmunity by naturally arising regulatory CD4+ T cells.
Naturally acquired immunological self-tolerance is not entirely accounted for by clonal deletion, anergy, and ignorance. It is now well established that the T cell-repertoire of healthy individuals harbors self-reactive lymphocytes with a potential to cause autoimmune disease and these lymphocytes are under dominant control by a unique subpopulation of CD4+ T cells now called regulatory T cells. Efforts to delineate these Treg cells naturally present in normal individuals have revealed that they are enriched in the CD25+ CD4+ population. The identification of the CD25 molecule as a useful marker for naturally arising CD4+ regulatory T cells has made it possible to investigate many key aspects of their immunobiology, including their antigen specificities and the cellular/molecular pathways involved in their development and their mechanisms of action. Furthermore, reduction or dysfunction of the CD25+ CD4+ regulatory T cell population can be responsible for certain autoimmune diseases in humans.
Hori
Shohei
S
Laboratory of Immunopathology, Research Center for Allergy and Immunology, The Institute for Physical and Chemical Research (RIKEN), Yokohama 230-0045, Japan.
Takahashi
Takeshi
T
Sakaguchi
Shimon
S
D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology; D015551:Autoimmunity; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D020869:Gene Expression Profiling; D006801:Humans; D008231:Lymphopenia / Q000276:immunology; D051379:Mice; D008822:Mice, Transgenic; D010641:Phenotype; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D017634:Self Tolerance; D016176:T-Lymphocyte Subsets / Q000276:immunology
D018925:Chemokines; D016207:Cytokines; D015375:Receptors, Interleukin-2