Abstract
The contribution of specific cell types to the production of cytokines that regulate hematopoiesis is still not well defined. We have previously identified T cell-dependent regulation of hematopoietic progenitor cell (HPC) numbers and cycling. In this report, we demonstrated that HPC activity is decreased in mice with STAT3-deficient T cells, a phenotype that is not because of decreased expression of IL-17 or RORγt. STAT3 expression in T cells was required for IL-21 production by multiple T helper subsets, and neutralization of IL-21 resulted in decreased HPC activity identical to that in mice with STAT3-deficient T cells. Importantly, injection of IL-21 rescued HPC activity in mice with STAT3-deficient T cells. Thus, STAT3-dependent IL-21 production in T cells is required for HPC homeostasis.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Gene Expression Regulation / genetics
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Gene Expression Regulation / immunology*
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Hematopoietic Stem Cells / cytology
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Hematopoietic Stem Cells / immunology*
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Hematopoietic Stem Cells / metabolism
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Homeostasis / genetics
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Homeostasis / immunology*
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Interleukin-17 / genetics
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Interleukin-17 / immunology
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Interleukin-17 / metabolism
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Interleukins / biosynthesis
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Interleukins / genetics
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Interleukins / immunology*
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Mice
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Mice, Knockout
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Nuclear Receptor Subfamily 1, Group F, Member 3 / genetics
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Nuclear Receptor Subfamily 1, Group F, Member 3 / immunology
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Nuclear Receptor Subfamily 1, Group F, Member 3 / metabolism
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STAT3 Transcription Factor / genetics
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STAT3 Transcription Factor / immunology*
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STAT3 Transcription Factor / metabolism
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T-Lymphocytes, Helper-Inducer / cytology
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T-Lymphocytes, Helper-Inducer / immunology*
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T-Lymphocytes, Helper-Inducer / metabolism
Substances
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Interleukin-17
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Interleukins
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Nuclear Receptor Subfamily 1, Group F, Member 3
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STAT3 Transcription Factor
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Stat3 protein, mouse
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interleukin-21