Jacobs M, Brown N, Allie N, Gulert R, Ryffel B
Department of Immunology, University of Cape Town, South Africa.
Immunology. 2000 Aug;100(4):494-501. doi: 10.1046/j.1365-2567.2000.00053.x.
Interleukin-10 (IL-10) down-regulates T helper type 1 cell and macrophage functions. As IL-10 is induced along with tumour necrosis factor (TNF) and IL-12 in mycobacterial infection, we asked whether endogenous IL-10 plays a role in the antimycobacterial response. We demonstrate here that IL-10-deficient mice eliminate Mycobacterium bovis Calmette-Guérin bacillus faster than wild-type mice. Granulomas are significantly larger, containing more CD-11b- and CD11c-positive antigen-presenting cells and T cells, and the expression of major histocompatibility complex class II and intracellular adhesion molecule-1 is increased. Macrophages in granulomas of IL-10-deficient mice express high levels of TNF, acid phosphatase and inducible nitric oxide synthase (iNOS). Finally, an increased cutaneous delayed-type hypersensitivity reaction to mycobacterial proteins is further evidence of an augmented cell-mediated immune response. In conclusion, the cell-mediated immunity is enhanced in the absence of IL-10, resulting in a robust granuloma response, which accelerates the clearance of mycobacteria. Therefore, endogenous IL-10 attenuates mycobacterial immunity.
白细胞介素-10（IL-10）可下调1型辅助性T细胞和巨噬细胞的功能。由于在分枝杆菌感染中IL-10与肿瘤坏死因子（TNF）和IL-12一起被诱导产生，我们研究内源性IL-10在抗分枝杆菌反应中是否发挥作用。我们在此证明，IL-10缺陷小鼠清除卡介苗牛型杆菌的速度比野生型小鼠更快。肉芽肿明显更大，含有更多CD-11b和CD11c阳性的抗原呈递细胞和T细胞，主要组织相容性复合体II类分子和细胞间黏附分子-1的表达增加。IL-10缺陷小鼠肉芽肿中的巨噬细胞表达高水平的TNF、酸性磷酸酶和诱导型一氧化氮合酶（iNOS）。最后，对分枝杆菌蛋白的皮肤迟发型超敏反应增强，进一步证明细胞介导的免疫反应增强。总之，在缺乏IL-10的情况下，细胞介导的免疫增强，导致强烈的肉芽肿反应，从而加速分枝杆菌的清除。因此，内源性IL-10会减弱分枝杆菌免疫。
