期刊
IMMUNITY
卷 28, 期 4, 页码 477-487出版社
CELL PRESS
DOI: 10.1016/j.immuni.2008.03.002
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资金
- Intramural NIH HHS [Z01 AR041106-13] Funding Source: Medline
- NCI NIH HHS [P30 CA21765, P30 CA021765] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P30CA021765] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [Z01AR041106, ZIAAR041159] Funding Source: NIH RePORTER
Cytokine signaling via a restricted number of Jak-Stat pathways positively and negatively regulates all cell types involved in the initiation, propagation, and resolution of inflammation. Here, we focus on Jak-Stat signaling in three major cell types involved in inflammatory responses: T cells, neutrophils, and macrophages. We summarize how the Jak-Stat pathways in these cells are negatively regulated by the Suppressor of cytokine signaling (Socs) proteins. We emphasize that common Jak-Stat-Socs signaling modules can have diverse developmental, pro- and anti-inflammatory outcomes depending on the cytokine receptor activated and which genes are accessible at a given time in a cell's life. Because multiple components of Jak-Stat-Socs pathways are mutated or closely associated with human inflammatory diseases, and cytokine-based therapies are increasingly deployed to treat inflammation, understanding cytokine signaling will continue to advance our ability to manipulate chronic and acute inflammatory diseases.
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