Calreticulin maintains the low threshold of peptide required for efficient antigen presentation
Calreticulin maintains the low threshold of peptide required for efficient antigen presentation
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钙网蛋白维持有效抗原呈递所需的肽的低阈值
DOI：
10.1016/j.molimm.2009.08.012
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发表时间：
2009-10-01
影响因子：
3.6
通讯作者：
Gao, Bin
中科院分区：
文献类型：
--
作者：
Fu, Hongmei;Liu, Changzhen;Gao, Bin
钙网蛋白（CRT）在MHC I类抗原加工和肽特异性CD8（+）T细胞抗肿瘤反应中起关键作用。然而，CRT如何有助于I类抗原加工及其在抗肿瘤反应中的佐剂作用机制仍有待阐明。在这里，我们表明，减少CRT缺陷细胞中的I类表达可以通过直接将肽递送到ER中或通过在低温下孵育来恢复。CRT缺陷型细胞在I类组装方面表现出TAP缺陷型表型，而不丧失TAP表达或功能。此外，细胞质中较高浓度的抗原是特异性T细胞刺激所必需的，这表明CRT在维持ER中有效抗原呈递所需的低肽浓度阈值方面具有功能性作用。在没有CRT的情况下，ERp57上调，这表明它们在I类抗原加工中相互协作。(C)2009爱思唯尔有限公司保留所有权利。
Calreticulin (CRT) plays a critical role in MHC class I antigen processing and elicits pepticle-specific CD8(+) T cell responses against tumours when administered with peptides. However, how CRT contributes to class I antigen processing and the mechanism of its adjuvant effect in anti-tumour responses, remain to be elucidated. Here we show that reduced class I expression in CRT deficient cells can be restored by the direct delivery of peptides into the ER or by incubation at low temperature. CRT deficient cells exhibited a TAP-deficient phenotype in terms of class I assembly, without loss of TAP expression or functionality. Furthermore, a higher concentration of antigen in the cytosol is required for specific T cell stimulation, suggesting that CRT has a functional role in the maintenance of the low peptide concentration threshold required in the ER for efficient antigen presentation. In the absence of CRT, ERp57 is up-regulated, which indicates that they collaborate with each other in class I antigen processing. (C) 2009 Elsevier Ltd. All rights reserved.