Ebert E C
Department of Medicine, UMDNJ Robert Wood Johnson Medical School, New Brunswick, NJ 08903, USA.
Clin Exp Immunol. 2000 Mar;119(3):426-32. doi: 10.1046/j.1365-2249.2000.01147.x.
IL-10 modulation of human intestinal T lymphocyte functions was studied for the first time. Lymphocyte proliferation was determined by 3H-thymidine incorporation; cytokine production, by ELISA; expression of surface markers, by immunofluorescence and flow cytometric analysis; and cytotoxicity, by lysis of 51Cr-labelled target cells. IL-10 blocked phytohaemagglutinin (PHA)-induced activation and proliferation of CD8+ T cells from the epithelium and lamina propria. It was a greater inhibitor of IL-2, interferon-gamma, and tumour necrosis factor-alpha production than were IL-4 or transforming growth factor-beta. In contrast, IL-10 enhanced IL-2-stimulated proliferation of both CD4+ and CD8+ T cells by increasing cell division after activation. It also augmented IL-2- but not IL-15-induced cytotoxicity of intestinal lymphocytes against colon cancer by a mechanism independent of natural killer cells. In conclusion, IL-10 blocking of proinflammatory cytokine secretion probably reduces intestinal inflammation. IL-10 augmentation of IL-2-induced cytotoxicity may help to maintain host defence.
首次对白细胞介素-10(IL-10)对人肠道T淋巴细胞功能的调节作用进行了研究。通过3H-胸腺嘧啶核苷掺入法测定淋巴细胞增殖;采用酶联免疫吸附测定法(ELISA)检测细胞因子产生;利用免疫荧光和流式细胞术分析检测表面标志物的表达;通过对51Cr标记靶细胞的裂解来检测细胞毒性。IL-10可阻断植物血凝素(PHA)诱导的来自上皮和固有层的CD8 + T细胞的活化和增殖。与IL-4或转化生长因子-β相比,它对IL-2、干扰素-γ和肿瘤坏死因子-α产生的抑制作用更强。相反,IL-10通过增加活化后的细胞分裂,增强了IL-2刺激的CD4 +和CD8 + T细胞的增殖。它还通过一种独立于自然杀伤细胞的机制增强了IL-2而非IL-15诱导的肠道淋巴细胞对结肠癌的细胞毒性。总之,IL-10对促炎细胞因子分泌的阻断可能会减轻肠道炎症。IL-10增强IL-2诱导的细胞毒性可能有助于维持宿主防御。