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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Blockade of tumour necrosis factor-α in experimental autoimmune encephalomyelitis reveals differential effects on the antigen-specific immune response and central nervous system histopathology
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Blockade of tumour necrosis factor-α in experimental autoimmune encephalomyelitis reveals differential effects on the antigen-specific immune response and central nervous system histopathology

机译：实验性自身免疫性脑脊髓炎对肿瘤坏死因子-α的阻断揭示了对抗原特异性免疫反应和中枢神经系统组织病理学的不同影响

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摘要

In various autoimmune diseases, anti-tumour necrosis factor (TNF)-α treatment has been shown to reduce both clinical disease severity and T helper type 1 (Th1)1/Th17 responses. In experimental autoimmune encephalomyelitis (EAE), however, the role of TNF-α has remained unclear. Here, C57BL/6 mice were immunized with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 and treated with anti-TNF-α, control antibody or vehicle. The clinical disease course, incidence and severity were assessed. On day 20 after immunization the antigen-specific Th1/Th17 response was evaluated by enzyme-linked immunospot (ELISPOT) in spleen and central nervous system (CNS). Also, the extent of spinal cord histopathology was analysed on semi- and ultrathin sections. Our results demonstrate that anti-TNF-α treatment reduced the incidence and delayed the onset of EAE, but had no effect on disease severity once EAE had been established. Whereas anti-TNF-α treatment induced an increase in splenic Th1/Th17 responses, there was no effect on the number of antigen-specific Th1/Th17 cells in the spinal cord. Accordingly, the degree of CNS histopathology was comparable in control and anti-TNF-α-treated mice. In conclusion, while the anti-TNF-α treatment had neither immunosuppressive effects on the Th1/Th17 response in the CNS nor histoprotective properties in EAE, it enhanced the myelin-specific T cell response in the immune periphery.
机译：在多种自身免疫性疾病中，抗肿瘤坏死因子（TNF）-α治疗已显示出可降低临床疾病严重程度和T辅助1型（Th1）1 / Th17反应。然而，在实验性自身免疫性脑脊髓炎（EAE）中，TNF-α的作用仍不清楚。在此，用髓磷脂少突胶质细胞糖蛋白（MOG）肽35-55免疫C57BL / 6小鼠，并用抗TNF-α，对照抗体或媒介物处理。评估临床疾病进程，发病率和严重程度。免疫后第20天，通过脾脏和中枢神经系统（CNS）中的酶联免疫斑点（ELISPOT）评估抗原特异性Th1 / Th17反应。同样，在半薄切片和超薄切片上分析了脊髓组织病理学的程度。我们的研究结果表明，抗TNF-α治疗可降低EAE的发生率并延缓EAE的发作，但是一旦建立EAE，对疾病的严重程度没有影响。尽管抗TNF-α治疗诱导脾脏Th1 / Th17反应增加，但对脊髓中抗原特异性Th1 / Th17细胞的数量没有影响。因此，在对照和抗TNF-α治疗的小鼠中，CNS组织病理学的程度可比。总之，尽管抗TNF-α处理对CNS中的Th1 / Th17反应既没有免疫抑制作用，也没有EAE中的组织保护作用，但它却增强了免疫外周的髓鞘特异性T细胞反应。

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