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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >The role of CD8+T cells and their local interaction with CD4+T cells in myelin oligodendrocyte glycoprotein35-55- induced experimental autoimmune encephalomyelitis
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The role of CD8+T cells and their local interaction with CD4+T cells in myelin oligodendrocyte glycoprotein35-55- induced experimental autoimmune encephalomyelitis

机译:CD8 + T细胞的作用及其与CD4 + T细胞的局部相互作用在髓鞘少突胶质细胞糖蛋白35-55诱导的实验性自身免疫性脑脊髓炎中的作用

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摘要

T cells have an essential role in the induction of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Although for CD4+T cells it is well established that they contribute to the disease, less is known about the role of CD8+T cells. Our aim was to determine the individual contribution of CD4+ and CD8+T cells in myelin oligodendrocyte glycoprotein (MOG)35-55-induced EAE. We investigated MOG35-55-activated CD8+T cells to clarify their potential to induce or attenuate EAE. We monitored the behavior of CD8 +T cells and their interaction with CD4+T cells directly at the site of inflammation in the CNS using intravital imaging of the brainstem of EAE-affected living anesthetized mice. We found that mice without CD4 +T cells did not develop relevant clinical signs of disease, although CD8+T cells were present in the CNS of these mice. These CD8 +T cells displayed reduced motility compared with those in the presence of CD4+T cells. In mice that harbored CD4+and CD8+T cells, we saw a similar extent of clinical signs of EAE as in mice with only CD4+T cells. Furthermore, the dynamic motility and viability of CD4+T cells were not disturbed by CD8+T cells in the lesions of these mice. Therefore, we conclude that in MOG35-55-induced EAE, CD8+T cell accumulation in the CNS represents instead an epiphenomenon with no impact on clinical disease or on the effects of CD4 +T cells, the latter being the true inducers of the disease.
机译:T细胞在诱导多发性硬化及其动物模型实验性自身免疫性脑脊髓炎(EAE)中起着至关重要的作用。尽管对于CD4 + T细胞,已经公认它们可导致疾病,但对CD8 + T细胞的作用知之甚少。我们的目的是确定髓鞘少突胶质细胞糖蛋白(MOG)35-55诱导的EAE中CD4 +和CD8 + T细胞的个体贡献。我们研究了MOG35-55激活的CD8 + T细胞,以阐明其诱导或减弱EAE的潜力。我们使用受EAE影响的活麻醉小鼠脑干的活体成像,直接在中枢神经系统炎症部位监测CD8 + T细胞的行为及其与CD4 + T细胞的相互作用。我们发现,尽管CD8 + T细胞存在于这些小鼠的中枢神经系统中,但没有CD4 + T细胞的小鼠却没有发展出相关的疾病临床症状。与存在CD4 + T细胞的那些相比,这些CD8 + T细胞显示出降低的运动性。在带有CD4 +和CD8 + T细胞的小鼠中,我们看到的EAE的临床体征与仅具有CD4 + T细胞的小鼠相似。此外,在这些小鼠的病变中,CD4 + T细胞的动态运动性和生存力不受CD8 + T细胞的干扰。因此,我们得出的结论是,在MOG35-55诱导的EAE中,CNS中CD8 + T细胞的积累代表了一种现象,对临床疾病或CD4 + T细胞的影响没有影响,后者是该疾病的真正诱因。

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