Differential T-cell activation by B7-1 expression.
Differential T-cell activation by B7-1 expression.
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B7-1 表达导致差异化 T 细胞激活。
DOI：
10.1046/j.1365-2567.2003.01658.x
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发表时间：
2003
期刊：
影响因子：
6.4
通讯作者：
Huber,BrigitteT
中科院分区：
文献类型：
--
作者：
Li,Wei;Rosenzweig,Anthony;Huber,BrigitteT
T细胞受体介导的T细胞活化需要共刺激信号，B7 - 1分子可以提供这种信号。我们先前的研究表明，通过重组腺病毒共表达共价肽/主要组织相容性复合物II类分子复合物和共刺激分子B7 - 1导致肽特异性T细胞活化的协同作用。然而，病毒抗原特异性T细胞活化并不被腺病毒表达的B7 - 1增强。为了验证B7 - 1对T细胞的不同激活作用并研究其潜在机制，我们构建了共表达鸡卵溶菌酶肽/I-Ak共价复合物的腺病毒，体内研究显示，由腺病毒介导的B7 - 1表达增强了HEL 46 -61特异性T细胞应答，但不增强病毒抗原特异性T细胞应答，这表明外源性B7 - 1表达可以通过不同的机制调节T细胞对这两种不同抗原的应答。此外，我们的研究结果表明，抗原呈递细胞在体内对腺病毒感染不敏感。基于这些发现，讨论了差异B7 - 1共刺激对肽特异性和病毒抗原特异性T细胞活化的可能机制。
T‐cell receptor‐mediated T‐cell activation requires cosimulation signal, which can be provided by B7‐1 molecule. Our previous study demonstrated that the coexpression of a covalent peptide/major histocompatibility complex class II molecule complex and costimulatory molecule B7‐1 by recombinant adenovirus leads to synergy in peptide‐specific T‐cell activation. However, the viral antigen‐specific T‐cell activation is not enhanced by B7‐1 expressed by the adenovirus. To verify the differential T cell activation by B7‐1 and investigate its underlying mechanisms, we constructed an adenovirus coexpressing a covalent complex of hen egg lysozyme peptide/I‐Ak(HEL46–61/I‐Ak) and B7‐1 in the present study.In vivostudies revealed that HEL46–61‐specific T‐cell response, but not viral antigen‐specific T‐cell response, was enhanced by B7‐1 expression mediated by the adenovirus, suggesting that exogenous B7‐1 expression may regulate T‐cell response to these two different antigens through distinct mechanisms. Furthermore, our results revealed that antigen‐presenting cells were unsusceptible to adenovirus infectionin vivo. Based on these findings, the possible mechanism of differential B7‐1 costimulation on peptide‐specific and viral antigen‐specific T‐cell activation is discussed.