[结节病肉芽肿形成机制——细胞因子和趋化因子的作用]

[Mechanism of sarcoid granuloma formation--participation of cytokines and chemokines].

作者信息

Sugiyama Yukihiko, Oshikawa Katsuhisa

机构信息

Division of Pulmonary Medicine, Department of Medicine, Jichi Medical School.

出版信息

Nihon Rinsho. 2002 Sep;60(9):1728-33.

PMID:12233067

Abstract

In sarcoidosis, unknown antigen(s) causes Th1-mediated granulomatous inflammation with cytokines such as IFN gamma and IL-12, initially. IL-16, IL-8, IP-10 and RANTES are participated in the accumulation of CD4+ T cell. For the chemotaxis of macrophages and monocytes, MCP-1, MIP1-alpha and RANTES are participated. Local proliferation of T cell is induced by IL-2 and IL-15 and that of macrophage/monocyte lineage is done by M-CSF, GM-CSF and G-CSF. Removal of the causative antigen(s) allows immune-suppressive cytokines such as TGF beta to downregulate the immune response and granuloma formation. Failure of removal of causative antigen(s) can induce prolonged existence of granuloma and irreversible fibrosis.

摘要

在结节病中，起初未知抗原引发由干扰素γ和白细胞介素12等细胞因子介导的Th1型肉芽肿性炎症。白细胞介素16、白细胞介素8、干扰素γ诱导蛋白10和调节激活正常T细胞表达和分泌的趋化因子参与CD4 + T细胞的聚集。对于巨噬细胞和单核细胞的趋化作用，单核细胞趋化蛋白1、巨噬细胞炎性蛋白1α和调节激活正常T细胞表达和分泌的趋化因子参与其中。白细胞介素2和白细胞介素15诱导T细胞局部增殖，而巨噬细胞/单核细胞系的增殖则由巨噬细胞集落刺激因子、粒细胞-巨噬细胞集落刺激因子和粒细胞集落刺激因子完成。去除致病抗原可使免疫抑制细胞因子如转化生长因子β下调免疫反应和肉芽肿形成。未能去除致病抗原可导致肉芽肿长期存在和不可逆纤维化。