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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Amelioration of experimental colitis by Copaxone is associated with class-II-restricted CD4 immune blocking.
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Amelioration of experimental colitis by Copaxone is associated with class-II-restricted CD4 immune blocking.

机译：Copaxone改善实验性结肠炎与II类限制的CD4免疫阻滞有关。

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Copaxone modifies TH1 immune response in multiple sclerosis. As Crohn's disease shares TH1 predominance, this study came to investigate the anti-inflammatory response of Copaxone in animal model of colitis. METHODS: Colitis was induced by intra-rectal instillation of TNBS in 2 animal groups; one of them was daily treated intraperitoneally by 300 mug Copaxone starting 48 h post-colitis induction. Both colitis groups were compared to naive group. Eight male C57Bl6 mice were used in each group. At day 12, distal colon was excised for standard scoring, splenocytes were isolated for FACS and serum cytokines were assessed. Splenocytes were in-vitro-stimulated with colitis protein extracts in the presence or absence of Copaxone. Lymphocytes were blocked by either MHC anti-class I or anti-class II antibodies prior to Copaxone administration. RESULTS: Copaxone markedly alleviated macro/microscopic colitis scoring as they decreased from 2.9 +/- 1.1/2.6 +/- 0.8 in colitis group to 1.7 +/- 1/1.5 +/- 0.5 in Copaxone-treated mice (P = 0.03/P = 0.008, respectively) compared to 0 +/- 0/1 +/- 0 in naives (P < 0.001/P < 0.01, respectively). CD4 subsets significantly decreased following Copaxone administration as compared to naive mice (P = 0.05). Although Copaxone-treated mice manifested a block of both serum TH1/TH2 responses, only interferon gamma secreting CD4 cells significantly decreased. NK cells tend to increase following colitis induction (P = 0.08), however, they significantly decreased in Copaxone-treated animals (P = 0.006). NK-T followed NK pattern. Using in vitro studies, Copaxone showed amelioration of T-cell proliferation that was significantly blocked when cells were pre-incubated with anti-MHC class II but not class I antibodies. CONCLUSIONS: Copaxone had class-II-restricted anti-inflammatory effect in our animal colitis model associated with CD4/NK/NKT/TH1/TH2 suppression.
机译：Copaxone可改变多发性硬化症的TH1免疫反应。由于克罗恩氏病具有TH1优势，因此本研究旨在研究结肠炎动物模型中Copaxone的抗炎反应。方法：通过直肠内滴注TNBS在2只动物组中诱发结肠炎。结肠炎诱导后48小时开始，每天用300杯Copaxone腹膜内治疗其中一位。将两个结肠炎组与幼稚组进行比较。每组使用八只雄性C57B16小鼠。在第12天，切除远端结肠用于标准评分，分离脾细胞进行FACS并评估血清细胞因子。在存在或不存在Copaxone的情况下，用结肠炎蛋白提取物体外刺激脾细胞。在给予Copaxone之前，淋巴细胞被MHC抗I类或抗II类抗体阻断。结果：Copaxone显着减轻了宏观/微观结肠炎评分，因为它们从结肠炎组的2.9 +/- 1.1 / 2.6 +/- 0.8降低至接受Copaxone治疗的小鼠的1.7 +/- 1 / 1.5 +/- 0.5（P = 0.03 /分别为P = 0.008）和朴素的0 +/- 0/1 +/- 0（分别为P <0.001 / P <0.01）。与未使用过的小鼠相比，服用Copaxone后的CD4亚群显着减少（P = 0.05）。尽管用Copaxone治疗的小鼠表现出两种血清TH1 / TH2反应均受阻，但只有干扰素γ分泌的CD4细胞显着降低。结肠炎诱导后，NK细胞趋于增加（P = 0.08），但是在用Copaxone治疗的动物中，NK细胞明显减少（P = 0.006）。 NK-T遵循NK模式。使用体外研究，Copaxone显示T细胞增殖的改善，当将细胞与抗MHC II类而非I类抗体进行预孵育时，T细胞增殖会明显受到抑制。结论：在我们的动物结肠炎模型中，与CD4 / NK / NKT / TH1 / TH2抑制有关，Copaxone具有II类限制性的抗炎作用。

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