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Modulation of MOG 37-50-specific CD8(+) T cell activation and expansion by CD43

机译:通过CD43调节MOG 37-50特异性CD8(+)T细胞的活化和扩增

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Several recent reports have described an effector role for CD8(+) T cells during EAE. We have previously demonstrated reduced disease incidence and severity in CD43(-/-) mice following MOG immunization, and attributed this attenuation in disease progression to the effects of CD43 deficiency on CD4(+) T cells. Here, we extend those studies to examine the effects of the loss of CD43 on MOG-specific CD8(+) T cells. A reduced frequency of MOG-specific CD8(+) T cells following immunization was observed in CD43(-/-) mice relative to wild-type controls, as demonstrated by intracellular cytokine and MHC tetramer staining. In addition, adoptive transfer of CD8(+) MOG 35-55-primed LN cells from CD43(-/-) mice resulted in significantly attenuated EAE induction as compared to recipients of wild-type CD8(+) MOG-primed cells. Analysis of intracellular signaling intermediates revealed a deficiency in the ability of MOG-specific CD8(+) T cells to phosphorylate ERK in response to antigen. These results characterize an important role for CD43 during the activation and expansion of autoreactive MOG-specific CD8(+) T cells. (c) 2006 Elsevier Inc. All rights reserved.
机译:最近的几篇报道描述了EAE期间CD8(+)T细胞的效应子作用。我们先前已经证明,MOG免疫后CD43(-/-)小鼠的疾病发病率和严重性降低,并且疾病进展的这种减弱归因于CD43缺乏对CD4(+)T细胞的影响。在这里,我们将那些研究扩展到检查CD43丢失对MOG特异性CD8(+)T细胞的影响。相对于野生型对照,在CD43(-/-)小鼠中观察到免疫后MOG特异性CD8(+)T细胞的频率降低,如细胞内细胞因子和MHC四聚体染色所证实。此外,与野生型CD8(+)MOG引发的细胞的受体相比,CD43(-/-)小鼠的CD8(+)MOG 35-55引发的LN细胞的过继转移导致EAE诱导显着减弱。细胞内信号转导中间体的分析表明,MOG特异性CD8(+)T细胞响应抗原而磷酸化ERK的能力不足。这些结果表征了CD43在活化和扩增自身反应性MOG特异性CD8(+)T细胞过程中的重要作用。 (c)2006 Elsevier Inc.保留所有权利。

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