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Publication : STAT5 is critical to maintain effector CD8+ T cell responses.

First Author  Tripathi P Year  2010
Journal  J Immunol Volume  185
Issue  4 Pages  2116-24
PubMed ID  20644163 Mgi Jnum  J:162623
Mgi Id  MGI:4819428 Doi  10.4049/jimmunol.1000842
Citation  Tripathi P, et al. (2010) STAT5 is critical to maintain effector CD8+ T cell responses. J Immunol 185(4):2116-24
abstractText  During an immune response, most effector T cells die, whereas some are maintained and become memory T cells. Factors controlling the survival of effector CD4(+) and CD8(+) T cells remain unclear. In this study, we assessed the role of IL-7, IL-15, and their common signal transducer, STAT5, in maintaining effector CD4(+) and CD8(+) T cell responses. Following viral infection, IL-15 was required to maintain a subpopulation of effector CD8(+) T cells expressing high levels of killer cell lectin-like receptor subfamily G, member 1 (KLRG1), and lower levels of CD127, whereas IL-7 and IL-15 acted together to maintain KLRG1(low)CD127(high) CD8(+) effector T cells. In contrast, effector CD4(+) T cell numbers were not affected by the individual or combined loss of IL-15 and IL-7. Both IL-7 and IL-15 drove phosphorylation of STAT5 within effector CD4(+) and CD8(+) T cells. When STAT5 was deleted during the course of infection, both KLRG1(high)CD127(low) and KLRG1(low)CD127(high) CD8(+) T cells were lost, although effector CD4(+) T cell populations were maintained. Furthermore, STAT5 was required to maintain expression of Bcl-2 in effector CD8(+), but not CD4(+), T cells. Finally, IL-7 and IL-15 required STAT5 to induce Bcl-2 expression and to maintain effector CD8(+) T cells. Together, these data demonstrate that IL-7 and IL-15 signaling converge on STAT5 to maintain effector CD8(+) T cell responses.
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