General nature of the STAT3-activated anti-inflammatory response
- Author(s)
- El Kasmi, KC; Holst, J; Coffre, M; Mielke, L; de Pauw, A; Lhocine, N; Smith, AM; Rutschman, R; Kaushal, D; Shen, Y; Suda, T; Donnelly, RP; Myers, MG; Alexander, W; Vignali, DAA; Watowich, SS; Ernst, M; Hilton, DJ; Murray, PJ;
- Details
- Publication Year 2006-12-01,Volume 177,Issue #11,Page 7880-7888
- Journal Title
- JOURNAL OF IMMUNOLOGY
- Publication Type
- Journal Article
- Abstract
- Although many cytokine receptors generate their signals via the STAT3 pathway, the IL-10R appears unique in promoting a potent anti-inflammatory response (AIR) via STAT3 to antagonize proinflammatory signals that activate the innate immune response. We found that heterologous cytokine receptor systems that activate STAT3 but are naturally refractory (the IL-22R), or engineered to be refractory (the IL-6, leptin, and erythropoietin receptors), to suppressor of cytokine signaling-3-mediated inhibition activate an AIR indistinguishable from IL-10. We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R.
- Publisher
- AMER ASSOC IMMUNOLOGISTS
- Keywords
- MICE LACKING STAT3; CYTOKINE SIGNALING-3; IN-VIVO; INTERLEUKIN-10 RECEPTOR; LEPTIN RECEPTOR; PROINFLAMMATORY CYTOKINE; CHRONIC ENTEROCOLITIS; FEEDBACK INHIBITION; HUMAN MACROPHAGES; IMMUNE-RESPONSES
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Creation Date: 2006-12-01 12:00:00