Abstract
Interleukin-15 receptor (IL-15R) contains α, β and γ chains. The α chain by itself binds to IL-15 with high affinity, while β and γ chains are intermediate affinity receptors for both Interleukin-2 (IL-2) and IL-15. Previous studies showed that mice deficient of IL-2 receptor α (IL-2Rα), IL-2/15 receptor β (IL-2/15Rβ) or IL-2 developed early progressing severe autoimmune diseases, a phenotype not observed in IL-15Rα knockout (IL-15Rα-/-) mice. We found that the Systemic Lupus Erythematosus (SLE)-like symptoms in female IL-15Rα-/- aged female mice older than 6 months but not in wild type (WT) counterpart. In this thesis, I demonstrated that IL-15Rα-/- mice exhibited inefficient tolerance in the thymus and in the periphery. These results may provide the mechanisms underlying the progressing autoimmune diseases in aged IL-15Rα-/- mice, which is the accumulation of autoimmune T cells resulted from inefficient immune tolerance.