Suga M, Yamasaki H, Nakagawa K, Kohrogi H, Ando M
First Department of Internal Medicine, Kumamoto University School of Medicine, Japan.
Sarcoidosis Vasc Diffuse Lung Dis. 1997 Sep;14(2):131-8.
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.
超敏反应性肉芽肿形成是过敏性肺炎（HP）的一种免疫病理特征。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迟发型超敏反应所诱发。先前致敏产生的循环性、抗原反应性记忆CD4+ T细胞，会响应趋化因子（如RANTES）迁移至肺实质。T细胞根据首次遇到抗原时的条件发育为Th0、Th1或Th2效应细胞。Th1细胞产生白细胞介素-2（IL-2）和干扰素-γ（IFN-γ）。IFN-γ可促使巨噬细胞转录并分泌更多的肿瘤坏死因子（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，如巨噬细胞活化因子（MAF）、巨噬细胞趋化因子（MCF）和巨噬细胞移动抑制因子（MIF）。这些单核因子将年轻巨噬细胞吸引至病变部位并激活它们，年轻巨噬细胞进而发育为成熟巨噬细胞，最终形成由上皮样细胞和多核巨细胞组成的超敏反应性肉芽肿。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。
