IL-2 and autoimmune disease.
A decade after the first description of IL-2-deficient mice, the redundancy of IL-2 as a T cell growth factor is well accepted and the focus of research has shifted to the unexpected multiorgan autoimmunity and inflammation observed in mice lacking components of the IL-2/IL-2R system. So far, a set of defects at the levels of repertoire selection, the generation of suppressive regulatory T cells, T cell homing and clonal contraction via activation induced cell death (AICD) have been documented. We propose that these individual defects jointly contribute to the severe disturbance of T cell homeostasis and self-tolerance underlying the immunopathology of the IL-2 deficiency syndrome.
Schimpl
Anneliese
A
Institute for Virology and Immunobiology, University of Würzburg, Versbacher Street 7, Würzburg D 97078, Germany. schimpl@vim.uni-wuerzburg.de
Berberich
Ingolf
I
Kneitz
Burkhardt
B
Krämer
Susanne
S
Santner-Nanan
Brigitte
B
Wagner
Sabine
S
Wolf
Martina
M
Hünig
Thomas
T
D000818:Animals; D017209:Apoptosis; D001327:Autoimmune Diseases / Q000235:genetics / Q000503:physiopathology*; D002465:Cell Movement; D017637:Clonal Deletion; D003713:Dendritic Cells / Q000276:immunology; D006706:Homeostasis; D006801:Humans; D007108:Immune Tolerance / Q000502:physiology; D007376:Interleukin-2 / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D008213:Lymphocyte Activation; D051379:Mice; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D015375:Receptors, Interleukin-2 / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D013577:Syndrome; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D019014:fas Receptor / Q000502:physiology
D007376:Interleukin-2; D015375:Receptors, Interleukin-2; D019014:fas Receptor