期刊
JOURNAL OF IMMUNOLOGY
卷 171, 期 11, 页码 5853-5864出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.171.11.5853
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资金
- NIAID NIH HHS [R01 AI050737-04, R01 AI050737-02, R01 AI050737-01A1, R01 AI050737-03, R21 AI050737-01, AI43620, R01 AI050737-05, AI05737] Funding Source: Medline
Using transgenic mice that express a constitutively active version of STAT5b, we demonstrate that STAT5 plays a key role in governing B cell development and T cell homeostasis. STAT5 activation leads to a 10-fold increase in pro-B, but not pro-T, cells. Conversely, STAT5 signaling promotes the expansion of mature alphabetaT cells (6-fold increase) and gammadelta and NK T cells (3- to 4-fold increase), but not of mature B cells. In addition, STAT5 activation has dramatically divergent effects on CD8(+) vs CD4(+) T cells, leading to the selective expansion of CD8(+) memory-like T cells and CD4(+)CD25(+) regulatory T cells. These results establish 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.
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