B7h, a novel costimulatory homolog of b7.1 and b7.2, is induced by TNFα
B7h, a novel costimulatory homolog of b7.1 and b7.2, is induced by TNFα
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DOI：
10.1016/s1074-7613(00)80117-x
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发表时间：
1999-10-01
期刊：
影响因子：
32.4
通讯作者：
Sha, WC
中科院分区：
文献类型：
--
作者：
Swallow, MM;Wallin, JJ;Sha, WC
在筛选NF-κ B/Rel转录因子诱导的基因时，我们克隆了一个新的基因b7 h，它是抗原呈递细胞上表达的B7共刺激配体的同源物。B7 h可以通过T细胞上不同于CD 28或CTLA-4的受体共刺激纯化的T细胞的增殖。令人惊讶的是，尽管B7 h在未刺激的B细胞中表达，但其表达在用TNF α处理的3 T3细胞和胚胎成纤维细胞中均被诱导，并且在用LPS（一种TNF α的有效激活剂）处理的小鼠的非淋巴组织中被上调。这些数据定义了一种新的T细胞共刺激配体，并表明TNF α诱导B7 h可能作为一种机制，直接增强炎症期间的自我识别。
In a screen to identify genes induced by NF-kappa B/Rel transcription factors, we cloned a novel gene, b7h, that is a close homolog of B7 costimulatory ligands expressed on antigen-presenting cells. B7h can costimulate proliferation of purified T cells through a receptor on T cells distinct from CD28 or CTLA-4. Surprisingly, although B7h is expressed in unstimulated B cells, its expression is induced in both 3T3 cells and embryonic fibroblasts treated with TNF alpha, and it is upregulated in nonlymphoid tissues of mice treated with LPS, a potent activator of TNF alpha. These data define a novel costimulatory ligand for T cells and suggest that induction of B7h by TNF alpha may function as a mechanism to directly augment recognition of self during inflammation.