Journal
SCIENCE
Volume 292, Issue 5523, Pages 1907-1910Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1059835
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- NEI NIH HHS [EY-07131] Funding Source: Medline
- NIAID NIH HHS [AI-42370] Funding Source: Medline
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How cytokines control differentiation of helper T (T-H) cells is controversial. We show that T-bet, without apparent assistance from interleukin 12 (IL-12)/ STAT4, specifies T(H)1 effector fate by targeting chromatin remodeling to individual interferon-gamma (IFN-gamma) alleles and by inducing IL-12 receptor beta2 expression. Subsequently, it appears that IL-12/STAT4 serves two essential functions in the development of T(H)1 cells: as growth signal, inducing survival and cell division; and as trans-activator, prolonging IFN-gamma synthesis through a genetic interaction with the coactivator, CREB-binding protein. These results suggest that a cytokine does not simply induce T-H fate choice but instead may act as an essential secondary stimulus that mediates selective survival of a lineage.
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