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IL-2 and autoimmune disease
Anneliese Schimpl1, Ingolf Berberich, Burkhardt Kneitz
1Institute for Virology and Immunobiology, University of Würzburg, Versbacher Street 7, Würzburg D 97078, Germany. schimpl@vim.uni-wuerzburg.de
Abstract:
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.