Matthew A. Burchill

TL;DR: Analysis of IL-2Rβ-dependent signal transduction pathways established that the transcription factor STAT5 is necessary and sufficient for Treg development, and ectopic expression of foxp3 in a subset of CD4+ T cells rescued T Reg development and prevented autoimmunity in IL- 2Rβ−/− mice.

TL;DR: It is demonstrated that expression of a constitutively active Stat5b transgene (Stat5b-CA) allowed for Treg cell development in neonatal mice and restored TReg cell numbers in Cd28(-/-) mice, which support a two-step model of Tregcell differentiation in which TCR and CD28 signals induce cytokine responsiveness and STAT5-inducing cytokines then complete the program of T Reg cell differentiation.

TL;DR: A distinct pattern of IL-2R signaling is found in which the Janus kinase/STAT pathway remains intact, whereasIL-2 does not activate downstream targets of phosphatidylinositol 3-kinase, which is inversely associated with expression of the phosphatase and tensin homologue deleted on chromosome 10, PTEN.

TL;DR: It is demonstrated that IL-2 plays the predominant role in Treg development, but that in its absence the IL-7Rα and IL-15Rα chains are up-regulated and allow for IL-9Rα or TSLPRα chains to partially compensate for loss ofIL-2.

TL;DR: It is established that activation of STAT5 is the primary mechanism underlying both IL-7/IL-15-dependent homeostatic proliferation of naive and memory CD8+ T cells and IL-2-dependent development of CD4+CD25+ regulatory T cells.