论文部分内容阅读
白细胞介素22(IL-22)是IL-10细胞因子家族成员之一,通过与IL-22R1、IL-10R2二聚体结合发挥作用。主要由T辅助细胞(T-helper cell)22(Th22)、Th17和Th1细胞表达,部分自然杀伤细胞(NK细胞)、γδT(T细胞受体的一种)细胞和淋巴组织可诱导(LTi)细胞也可表达。结核性胸腔积液和恶性胸腔积液中都存在显著升高的IL-22,主要来源于受趋化因子作用募集于胸膜腔的外周血CD4+T淋巴细胞和胸膜腔局部在IL-6、IL-23、IL-1β和肿瘤坏死因子-α(TNF-α)等细胞因子作用下分化而来的CD4+T细胞。在胸膜腔中,IL-22通过促进基质金属蛋白酶(matrix metalloproteinases,MMPs)的表达发挥免疫病理作用,并通过介导NK细胞产生溶解因子减少寄生于单核细胞来源的巨噬细胞内的结核分枝杆菌生长。在恶性胸腔积液中,IL-22可通过促进肿瘤细胞增殖、迁移,并且通过增加黏附分子的表达促进与胸膜间皮细胞(pleural mesothelial cells,PMCs)的黏附发挥作用。研究IL-22在上述两种疾病中的作用机制,将会为免疫诊断与治疗开辟新的途径。
Interleukin-22 (IL-22), a member of the IL-10 cytokine family, functions by binding to the IL-22R1, IL-10R2 dimer. It is mainly induced by T-helper cell 22 (Th22), Th17 and Th1 cells, partly natural killer cells (NK cells), γδT (a T cell receptor) cell and lymphoid tissue can be induced (LTi) Cells are also expressed. Tuberculous pleural effusion and malignant pleural effusion were significantly elevated IL-22, mainly from chemokine action raised in the pleural cavity of peripheral blood CD4 + T lymphocytes and pleural cavity local in IL-6, IL-23, IL-1β and tumor necrosis factor-α (TNF-α) and other cytokines under the differentiation of CD4 + T cells. In the pleural cavity, IL-22 exerts an immunopathogenic effect by promoting the expression of matrix metalloproteinases (MMPs) and reduces the tuberculosis that is parasitic in monocyte-derived macrophages by mediating the production of lytic factors by NK cells Mycobacterial growth. In malignant pleural effusion, IL-22 can promote the proliferation and migration of tumor cells and promote the adhesion with pleural mesothelial cells (PMCs) by increasing the expression of adhesion molecules. Studying the mechanism of action of IL-22 in the above two diseases will open up new avenues for immune diagnosis and treatment.