期刊
IMMUNITY
卷 27, 期 1, 页码 100-110出版社
CELL PRESS
DOI: 10.1016/j.immuni.2007.04.018
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资金
- NCI NIH HHS [R01 CA092433, R01 CA092433-05, P01 CA119070, P01 CA119070-01A19001, P01 CA119070-020003] Funding Source: Medline
- NIAID NIH HHS [R01 AI047833-09, R01 AI047833] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007229, T32GM007229] Funding Source: Medline
Notch signaling plays multiple roles to direct diverse decisions regarding cell fate during T cell development. During helper T (Th) cell differentiation, Notch is involved in generating optimal Th2 cell responses. Here, we present data investigating how Notch mediates Th2 cell differentiation. Notch showed a CD4+ T cell intrinsic role in promoting IL-4 expression that required GATA-3. In the absence of Notch signals, Gata3 expression was markedly diminished. Introduction of an activated allele of Notchl into CD4+ T cells led to the specific and direct upregulation of a developmentally regulated Gata3 transcript that included the exon 1a sequences. Furthermore, Notch acted in parallel with GATA-3 to synergistically activate IL-4 expression. Together, these data implicate Gata3 as a direct transcriptional Notch target that acts in concert with Notch signaling to generate optimal Th2 cell responses.
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