Cytokine Growth Factor Rev 2002 Aug;13(4-5):369
Schimpl A, Berberich I, Kneitz B, Kramer S, Santner-Nanan B, Wagner S, Wolf M, Hunig T.
Institute for Virology and Immunobiology, University of Wurzburg, Versbacher Street 7, D 97078, Wurzburg, Germany
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.