Mechanisms accounting for granulomatous responses in hypersensitivity pneumonitis.
Mechanisms accounting for granulomatous responses in hypersensitivity pneumonitis.
复制标题
过敏性肺炎肉芽肿反应的机制。
DOI：
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发表时间：
1997
期刊：
影响因子：
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通讯作者：
M. Ando
中科院分区：
文献类型：
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作者：
Moritaka Suga;Hisato Yamasaki;Kazuko Nakagawa;H. Kohrogi;M. Ando
过敏性肉芽肿形成是HP的免疫病理特征。它是由T细胞介导的对侵入肺部的有机粉尘或活性化学物质的延迟型超敏反应引起的。由先前致敏产生的循环、抗原反应性、记忆性CD4+ T细胞在趋化因子如RANTES的作用下迁移到肺实质。T细胞发育成Th0、Th1或Th2效应细胞取决于它们第一次遇到抗原的条件。Th1细胞产生IL-2和ifn - γ。ifn - γ可以诱导巨噬细胞转录并分泌更多的TNF和IL-1。被TNF和IL-1激活的巨噬细胞产生多种生物活性介质，如MAF、MCF和MIF。这些单因子吸引年轻的巨噬细胞进入病变，激活它们，年轻的巨噬细胞发育成成熟的巨噬细胞，导致由上皮样细胞和多核巨细胞组成的超敏性肉芽肿。CD8+ T细胞是HP病变中最主要的细胞，可能通过产生th1样或th2样细胞因子来调节肉芽肿的形成。
Hypersensitivity granuloma formation is an immunopathological feature of HP. It is induced by the T cell-mediated delayed-type hypersensitivity reaction to organic dusts or active chemicals invading the lung. Circulating, antigen-reactive, memory CD4+ T cells, generated by previous sensitization, migrate into lung parenchyma in response to chemokines such as RANTES. The T cells develop into either Th0, Th1, or Th2 effector depending upon the conditions in which they first encounter the antigens. The Th1 cells produce IL-2 and IFN-gamma. IFN-gamma can prime macrophages to transcribe and to secrete greater amounts of TNF and IL-1. The macrophages activated by TNF and IL-1 produce a wide range of biologically active mediators such as MAF, MCF, and MIF. These monokines attract young macrophages into the lesions, activate them, and young macrophages develop into mature macrophages, resulting in the hypersensitivity granuloma consisting of epithelioid cells and multinucleated giant cells. CD8+ T cells, the most predominant cell in the lesions of HP, may modulate the granuloma formation via the production of Th1-like or Th2-like cytokines.