IL-2 and autoimmune disease

摘要: A decade after the first description of IL-2-deficient mice, redundancy IL-2 as a T cell growth factor is well accepted and focus research has shifted to unexpected multiorgan autoimmunity inflammation observed in mice lacking components IL-2/IL-2R system. So far, set defects at levels repertoire selection, generation suppressive regulatory cells, homing clonal contraction via activation induced death (AICD) have been documented. We propose that these individual jointly contribute severe disturbance homeostasis self-tolerance underlying immunopathology deficiency syndrome.