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包含逆转录病毒包膜糖蛋白免疫抑制结构域的肽的抗原性。

Antigenicity of peptides comprising the immunosuppressive domain of the retroviral envelope glycoprotein.

作者信息

Jenkins Bryony, Eksmond Urszula, Young George, Kassiotis George

机构信息

The Francis Crick Institute, London, UK.

Department of Medicine, Faculty of Medicine, Imperial College London, London, UK.

出版信息

Wellcome Open Res. 2016 Dec 6;1:22. doi: 10.12688/wellcomeopenres.10269.2.

Abstract

To achieve persistent infection of the host, viruses often subvert or suppress host immunity through mechanisms that are not entirely understood. The envelope glycoprotein of several retroviruses is thought to possess potent immunosuppressive activity, mapped to a 17-amino acid residue conserved domain. Synthetic peptides corresponding to this immunosuppressive domain can inhibit lymphocyte activation, whereas mutation of key domain residues can increase the lymphocyte response to linked antigenic epitopes. Using three T cell receptors (TCRs) of defined specificity, we examine the effect of the immunosuppressive domain on the T cell response to their respective antigenic peptides. We find that fusion of a T cell epitope to the immunosuppressive domain can greatly modulate its potency. However, the effects heavily depend on the particular combination of TCR and peptide-major histocompatibility complex class II (pMHC II), and are mimicked by sequence-scrambled peptides of similar length, suggesting they operate at the level of TCR-pMHC interaction. These results offer an alternative explanation for the immunogenicity of T cell epitopes comprising the putative immunosuppressive domain, which is more consistent with an effect on peptide antigenicity than true immunosuppressive activity.

摘要

为实现对宿主的持续感染,病毒常常通过一些尚未完全明确的机制来颠覆或抑制宿主免疫。几种逆转录病毒的包膜糖蛋白被认为具有强大的免疫抑制活性,该活性定位于一个由17个氨基酸残基组成的保守结构域。与这个免疫抑制结构域相对应的合成肽能够抑制淋巴细胞活化,而关键结构域残基的突变则可增强淋巴细胞对相连抗原表位的反应。我们利用三种具有明确特异性的T细胞受体(TCR),研究了免疫抑制结构域对T细胞针对其各自抗原肽反应的影响。我们发现,将一个T细胞表位与免疫抑制结构域融合可极大地调节其效力。然而,这些效应在很大程度上取决于TCR与肽 - 主要组织相容性复合体II类(pMHC II)的特定组合,并且被长度相似的序列打乱的肽所模拟,这表明它们在TCR - pMHC相互作用层面发挥作用。这些结果为包含假定免疫抑制结构域的T细胞表位的免疫原性提供了另一种解释,这与对肽抗原性的影响比真正的免疫抑制活性更为一致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308f/5446027/d59b40b840cf/wellcomeopenres-1-11822-g0000.jpg

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