Abstract
How cytokines control differentiation of helper T (TH) cells is controversial. We show that T-bet, without apparent assistance from interleukin 12 (IL-12)/STAT4, specifies TH1 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 TH1 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 TH fate choice but instead may act as an essential secondary stimulus that mediates selective survival of a lineage.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alleles
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Animals
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CREB-Binding Protein
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Cell Differentiation
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Cell Division
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Cell Lineage
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Cells, Cultured
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DNA-Binding Proteins / metabolism
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Gene Expression Regulation
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Histones / metabolism
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Interferon-gamma / biosynthesis*
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Interferon-gamma / genetics
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Interleukin-12 / metabolism*
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Lymphocyte Activation
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Nuclear Proteins / metabolism
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Receptors, Interleukin / metabolism
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Receptors, Interleukin-12
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STAT4 Transcription Factor
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Signal Transduction
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T-Box Domain Proteins
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Th1 Cells / cytology
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Th1 Cells / immunology*
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Th1 Cells / metabolism
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Trans-Activators / metabolism
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Transcription Factors / genetics
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Transcription Factors / metabolism*
Substances
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DNA-Binding Proteins
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Histones
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Il12rb2 protein, mouse
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Nuclear Proteins
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RNA, Messenger
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Receptors, Interleukin
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Receptors, Interleukin-12
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STAT4 Transcription Factor
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Stat4 protein, mouse
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T-Box Domain Proteins
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T-box transcription factor TBX21
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Trans-Activators
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Transcription Factors
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Interleukin-12
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Interferon-gamma
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CREB-Binding Protein
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Crebbp protein, mouse