期刊
JOURNAL OF IMMUNOLOGY
卷 178, 期 11, 页码 6705-6709出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.11.6705
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资金
- NIAID NIH HHS [R01 AI069120, R01 AI056154, R37 AI47868] Funding Source: Medline
Macrophages respond to LPS hy the rapid activation of proinflammatory cytokines that serve to initiate host defense against microbial invasion. To prevent injury to the host from excess production of these cytokines, IL-10 is upregulated to feedback inhibit the proinflammatory response. However, the molecular events responsible for LPS-induced up-regulation of IL-10 remain to be elucidated. In this study, we provide evidence that production of and signaling by type IIFN is required for LPS-induced IL-10 up-regulation. In addition, we demonstrate that defect in type I IFN production and signaling results in a trend toward LPS-mediated superinduction of proinflammatory genes and cytokines in bone marrow-derived macrophages. Our findings suggest a novel antiinflammatory role for the type I IFN production and signaling pathway in regulating LPS response in bone marrow-derivedmacrophages.
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