首页> 外文期刊>Neurobiology of disease >Mouse Schwann cells activate MHC class I and II restricted T-cell responses, but require external peptide processing for MHC class II presentation.
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Mouse Schwann cells activate MHC class I and II restricted T-cell responses, but require external peptide processing for MHC class II presentation.

机译:小鼠雪旺氏细胞激活MHC I类和II类限制的T细胞反应,但需要进行MHC II类提呈的外部肽加工。

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摘要

Schwann cells are the myelinating glia cells of the peripheral nervous system (PNS). In inflammatory neuropathies like the Guillain-Barre syndrome (GBS) Schwann cells become target of an autoimmune response, but may also modulate local inflammation. Here, we tested the functional relevance of Schwann cell derived MHC expression in an in vitro coculture system. Mouse Schwann cells activated proliferation of ovalbumin specific CD8+ T cells when ovalbumin protein or MHC class I restricted ovalbumin peptide (Ova(257-264) SIINFEKL) was added and after transfection with an ovalbumin coding vector. Schwann cells activated proliferation of ovalbumin specific CD4+ T cells in the presence of MHC class II restricted ovalbumin peptide (Ova(323-339) ISQAVHAAHAEINEAGR). CD4+ T-cell proliferation was not activated by ovalbumin protein or transfection with an ovalbumin coding vector. This indicates that Schwann cells express functionally active MHC class I and II molecules. In this study, however, Schwann cells lacked the ability to process exogenous antigen or cross-present endogenous antigen into the MHC class II presentation pathway. Thus, antigen presentation may be a pathological function of Schwann cells exacerbating nerve damage in inflammatory neuropathies.
机译:雪旺氏细胞是周围神经系统(PNS)的髓质胶质细胞。在诸如吉兰-巴利综合征(GBS)的炎性神经病中,雪旺氏细胞成为自身免疫反应的靶标,但也可能调节局部炎症。在这里,我们测试了在体外共培养系统中雪旺细胞衍生的MHC表达的功能相关性。当添加卵清蛋白蛋白或MHC I类限制性卵清蛋白肽(Ova(257-264)SIINFEKL)并用卵清蛋白编码载体转染后,小鼠雪旺细胞激活卵清蛋白特异性CD8 + T细胞的增殖。在MHC II类限制性卵白蛋白肽(Ova(323-339)ISQAVHAAHAEINEAGR)存在下,许旺细胞激活卵白蛋白特异性CD4 + T细胞的增殖。卵清蛋白蛋白或用卵清蛋白编码载体转染不会激活CD4 + T细胞增殖。这表明雪旺氏细胞表达具有功能活性的MHC I类和II类分子。然而,在这项研究中,雪旺氏细胞缺乏将外源抗原或交叉呈递的内源性抗原加工成MHC II类呈递途径的能力。因此,抗原呈递可能是雪旺氏细胞的病理功能,加剧了炎性神经病中的神经损伤。

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