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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Redundancy renders the glycoprotein 96 receptor scavenger receptor A dispensable for cross priming in vivo.
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Redundancy renders the glycoprotein 96 receptor scavenger receptor A dispensable for cross priming in vivo.

机译：冗余使得糖蛋白96受体清除剂受体A可以在体内交叉引发。

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摘要

CD8(+) T cells (T(CD8+)) differentiate into effector cells following recognition of specific peptide-major histocompatibility complex (MHC) class I complexes (pMHC-I) on the surface of professional APCs (pAPCs), such as dendritic cells. Antigenic pMHC-I can be generated from two spatially distinct sources. The direct presentation pathway involves generation of peptide from protein substrate synthesized within the cell that is presenting the pMHC-I. Alternatively, the cross presentation pathway involves presentation of antigen that is not synthesized within the presenting cell, but is derived from exogenous proteins synthesized within other donor cells. The mechanisms by which cross presentation of exogenous antigens occur in vivo remain controversial. The C-type lectin scavenger receptor A (SR-A) has been implicated in a number of potential cross presentation pathways, including the presentation of peptide bound to heat shock proteins, such as glycoprotein 96 (gp96), and the transfer of pMHC-I from a donor cell to the pAPC. We demonstrate here that initiation of T(CD8+) responses is normal in mice lacking SR-A, and that the redundancy of ligand binding exhibited by the SR family is likely to be an important mechanism that ensures cross presentation in vivo. These observations emphasize the requirement to target multiple receptors and antigen-processing pathways during the rational design of vaccines aimed at eliciting protective T(CD8+).
机译：CD8（+）T细胞（T（CD8 +））在识别树突状细胞等专业APC（pAPC）表面上的特定肽-主要组织相容性复合物（MHC）I类复合物（pMHC-I）之后，分化成效应细胞。抗原pMHC-1可以从两个空间不同的来源生成。直接呈递途径涉及从呈递pMHC-1的细胞内合成的蛋白质底物生成肽。或者，交叉呈递途径涉及呈递细胞中未合成但来自其他供体细胞中合成的外源蛋白质的抗原的呈递。在体内发生外源抗原交叉呈递的机制仍存在争议。 C型凝集素清除剂受体A（SR-A）与许多潜在的交叉呈递途径有关，包括呈递与热激蛋白结合的肽，例如糖蛋白96（gp96），以及pMHC-我从供体细胞到pAPC。我们在这里证明缺乏SR-A的小鼠中T（CD8 +）反应的启动是正常的，并且SR家族所表现出的配体结合的冗余很可能是确保体内交叉呈递的重要机制。这些观察结果强调了在合理设计旨在引发保护性T（CD8 +）的疫苗过程中，针对多种受体和抗原加工途径的要求。

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