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lüll Cytokine signaling modules in inflammatory responses O'Shea JJ; Murray PJImmunity 2008[Apr]; 28 (4): 477-87Cytokine 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.|Animals[MESH]|Cytokines/genetics/metabolism/*physiology[MESH]|Humans[MESH]|Inflammation Mediators/metabolism/*physiology[MESH]|Neutrophils/enzymology/*immunology/metabolism/*pathology[MESH]|Receptors, Cytokine/genetics/metabolism/physiology[MESH]|STAT Transcription Factors/genetics/metabolism/physiology[MESH]|Signal Transduction/genetics/*immunology[MESH]|Suppressor of Cytokine Signaling Proteins/genetics/metabolism/physiology[MESH]|T-Lymphocytes/enzymology/*immunology/metabolism/*pathology[MESH] |