国产bbaaaaa片,成年美女黄网站色视频免费,成年黄大片,а天堂中文最新一区二区三区,成人精品视频一区二区三区尤物

首頁> 美國衛(wèi)生研究院文獻>Blood >Chemokines Cytokines and Interleukins: Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice
【2h】

Chemokines Cytokines and Interleukins: Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice

機譯：趨化因子細胞因子和白介素：肥大細胞源性TNF可以促進卵白蛋白攻擊的OTII小鼠中Th17細胞依賴性中性粒細胞的募集

代理獲取
本網站僅為用戶提供外文OA文獻查詢和代理獲取服務，本網站沒有原文。下單后我們將采用程序或人工為您竭誠獲取高質量的原文，但由于OA文獻來源多樣且變更頻繁，仍可能出現(xiàn)獲取不到、文獻不完整或與標題不符等情況，如果獲取不到我們將提供退款服務。請知悉。
  • 摘要
  • 著錄項
  • 相似文獻
  • 相關主題

摘要

Both mast cells and IL-17 can contribute to host defense and pathology in part by orchestrating neutrophil recruitment, but the possible role of mast cells in IL-17–induced inflammation remains to be defined. We found that mast cells and IL-17, but neither IFN-γ nor FcRγ signaling, contributed significantly to the antigen (Ag)–dependent airway neutrophilia elicited in ovalbumin-specific T-cell receptor (TCR)–expressing C57BL/6-OTII mice, and that IFN-γ significantly suppressed IL-17–dependent airway neutrophilia in this setting. IL-18, IL-1β, and TNF each contributed significantly to the development of Ag- and T helper 17 (Th17 cell)–mediated airway neutrophilia. Moreover, IL-17 enhanced mast cell TNF production in vitro, and mast cell–associated TNF contributed significantly to Ag- and Th17 cell–mediated airway neutrophilia in vivo. By contrast, we detected no significant role for the candidate mediators histamine, PGD2, LTB4, CXCL10, or IL-16, each of which can be produced by mast cells and other cell types, in the neutrophil infiltration elicited in this model. These findings establish that mast cells and mast cell–derived TNF can significantly enhance, by FcRγ-independent mechanisms, the Ag- and Th17 cell–dependent development of a neutrophil-rich inflammatory response at a site of Ag challenge.
機譯：肥大細胞和IL-17均可部分通過編排中性粒細胞募集而有助于宿主防御和病理，但肥大細胞在IL-17誘導的炎癥中的可能作用尚待確定。我們發(fā)現(xiàn)肥大細胞和IL-17，但沒有IFN-γ和FcRγ信號傳導，對表達卵白蛋白特異性T細胞受體（TCR）的C57BL / 6-OTII誘導的抗原（Ag）依賴性氣道中性粒細胞顯著貢獻在這種情況下，IFN-γ可以顯著抑制依賴IL-17的氣道中性粒細胞增多。 IL-18，IL-1β和TNF分別對由Ag和T輔助17（Th17細胞）介導的氣道中性粒細胞的形成做出了重要貢獻。此外，IL-17增強了體外肥大細胞TNF的產生，而肥大細胞相關的TNF在體內顯著促進了Ag和Th17細胞介導的氣道中性粒細胞增多。相比之下，在該模型引起的嗜中性粒細胞浸潤中，我們未檢測到組胺，PGD2，LTB4，CXCL10或IL-16的候選介體的重要作用，組胺，PGD2，LTB4，CXCL10或IL-16均可由肥大細胞和其他細胞類型產生。這些發(fā)現(xiàn)表明，肥大細胞和肥大細胞衍生的TNF可以通過FcRγ依賴性機制顯著增強Ag攻擊位點上富含嗜中性白細胞的炎癥反應的Ag和Th17細胞依賴性發(fā)育。

著錄項

相似文獻

  • 外文文獻
  • 中文文獻
  • 專利
代理獲取

客服郵箱：kefu@zhangqiaokeyan.com

京公網安備：11010802029741號 ICP備案號：京ICP備15016152號-6 六維聯(lián)合信息科技 (北京) 有限公司?版權所有

  • 客服微信

  • 服務號