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在肺部炎症效应阶段,Th2诱导的嗜酸性粒细胞趋化因子表达和嗜酸性粒细胞增多与Th1反应共存。

Th2-induced eotaxin expression and eosinophilia coexist with Th1 responses at the effector stage of lung inflammation.

作者信息

Li L, Xia Y, Nguyen A, Feng L, Lo D

机构信息

Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.

出版信息

J Immunol. 1998 Sep 15;161(6):3128-35.

PMID:9743380
Abstract

The T cell-mediated lung inflammation that is associated with allergic asthma is characterized mainly by massive eosinophil infiltration, which induces airway injury and the subsequent late-phase reactivity. Because Th2 cells are often isolated from asthmatic subjects, these cells are postulated to play a role in asthma pathogenesis. We report that adoptively transferred, influenza hemagglutinin-specific Th1 and Th2 cells induced different patterns of chemokines leading to different types of cellular infiltration. Th2 cells were sufficient to induce dramatic Ag-dependent lung eosinophilia and eotaxin expression; by contrast, Th1 transfer primarily induced neutrophil recruitment with little eotaxin production. To determine whether Th1 cells show inhibitory effects on Th2 cell-mediated responses, Th1 and Th2 cells were cotransferred. Hemagglutinin-specific Th1 cells did not inhibit Ag-induced lung eosinophilia, nor did they inhibit eotaxin expression. Furthermore, influenza virus infection of the lung in mice receiving hemagglutinin-specific Th2 cells also induced eotaxin expression and eosinophilia that could not be inhibited by the cotransfer of Th1 cells. Our results show that Th2-mediated allergic lung inflammation coexists with the Th1-mediated responses that are stimulated by diverse forms of Ags.

摘要

与过敏性哮喘相关的T细胞介导的肺部炎症主要特征为大量嗜酸性粒细胞浸润,这会导致气道损伤及随后的迟发相反应。由于经常从哮喘患者体内分离出Th2细胞,因此推测这些细胞在哮喘发病机制中发挥作用。我们报告称,过继转移的流感血凝素特异性Th1和Th2细胞诱导出不同模式的趋化因子,导致不同类型的细胞浸润。Th2细胞足以诱导显著的抗原依赖性肺部嗜酸性粒细胞增多和嗜酸性粒细胞趋化因子表达;相比之下,Th1细胞转移主要诱导中性粒细胞募集,几乎不产生嗜酸性粒细胞趋化因子。为了确定Th1细胞是否对Th2细胞介导的反应具有抑制作用,将Th1和Th2细胞共同转移。血凝素特异性Th1细胞既不抑制抗原诱导的肺部嗜酸性粒细胞增多,也不抑制嗜酸性粒细胞趋化因子表达。此外,接受血凝素特异性Th2细胞的小鼠肺部感染流感病毒也会诱导嗜酸性粒细胞趋化因子表达和嗜酸性粒细胞增多,而Th1细胞的共同转移无法抑制这一现象。我们的结果表明,Th2介导的过敏性肺部炎症与由多种形式抗原刺激引发的Th1介导的反应共存。

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