Abstract
The interleukin-1 (IL-1) superfamily of cytokines comprises a set of pivotal mediators of inflammation. Among them, the action of IL-36 cytokines in immune responses has remained elusive. In a recent study, we demonstrated a direct effect of IL-36 on immune cells. Here we show that, among T cells, the IL-36 receptor is predominantly expressed on naive CD4(+) T cells and that IL-36 cytokines act directly on naive T cells by enhancing both cell proliferation and IL-2 secretion. IL-36β acts in synergy with IL-12 to promote Th1 polarization and IL-36 signaling is also involved in mediating Th1 immune responses to Bacillus Calmette-Guerin infection in vivo. Our findings point toward a critical function of IL-36 in the priming of Th1 cell responses in vitro, and in adaptive immunity in a model of mycobacterial infection in vivo.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptive Immunity
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Animals
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Cell Differentiation
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Cell Proliferation
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Interleukin-1 / immunology
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Interleukin-1 / pharmacology
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Interleukin-12 / immunology
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Interleukin-12 / pharmacology
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Interleukin-2 / biosynthesis
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Interleukin-2 / immunology
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Lymphocyte Activation
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Mice
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Mice, Knockout
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Mycobacterium bovis / immunology*
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Primary Cell Culture
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Receptors, Interleukin-1 / deficiency
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Receptors, Interleukin-1 / genetics
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Receptors, Interleukin-1 / immunology*
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Signal Transduction / genetics
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Signal Transduction / immunology*
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Th1 Cells / cytology
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Th1 Cells / immunology*
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Th1 Cells / microbiology
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Tuberculosis / genetics
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Tuberculosis / immunology
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Tuberculosis / metabolism*
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Tuberculosis / veterinary*
Substances
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IL-1F8 protein, mouse
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Interleukin-1
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Interleukin-2
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Receptors, Interleukin-1
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interleukin 1F6, mouse
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interleukin-36 receptor, mouse
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Interleukin-12