期刊
NATURE IMMUNOLOGY
卷 12, 期 4, 页码 327-U80出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1996
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资金
- US National Institutes of Health [AI-15608, HL-33391, AI-37293, U19 AI-083024]
- University of Virginia Center for Immunity, Inflammation and Regenerative Medicine
- American Lung Association [RN-123000]
Interleukin (IL)-10 is an important regulatory cytokine that can modulate excessive immune mediated injury. Several distinct cell types have been demonstrated to produce IL-10, including most recently CD8(+) cytotoxic T lymphocytes (CTLs) responding to respiratory virus infection. Here we report that CD4(+) T cell help in the form of IL-2 is required for IL-10 production by CTLs, but not for the induction of CTL effector cytokines. We show that IL-2 derived from CD4(+) helper T cells cooperates with innate immune cell-derived IL-27 to amplify IL-10 production by CTLs through a Blimp-1-dependent mechanism. These findings reveal a previously unrecognized pathway that coordinates signals derived from innate and helper T cells to control the production of a regulatory cytokine by CTLs during acute viral infection.
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