Herpesvirus Saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor
Herpesvirus Saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor
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DOI：
10.1016/1074-7613(95)90070-5
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发表时间：
1995-12-01
期刊：
影响因子：
32.4
通讯作者：
Spriggs, MK
中科院分区：
文献类型：
--
作者：
Yao, ZB;Fanslow, WC;Spriggs, MK
疱疹病毒Saimiri基因13(HVS13)与T细胞衍生分子CTLA8的预测序列有57%的同源性。重组HVS13和CTLA8可刺激成纤维细胞转录因子NF-kappaB活性和IL-6的分泌，并协同刺激T细胞增殖。用一个HVS13.Fc融合蛋白来分离编码一种新的受体的cDNA，该受体也与CTLA8结合。该受体与先前发现的细胞因子受体家族无关。重组可溶性受体可抑制PHA、刀豆蛋白A(ConA)和抗TCR单抗诱导的T细胞增殖和IL-2的产生。这些结果将CTLA8和HVS13定义为与新的细胞因子受体结合的新的细胞因子。我们建议将这些分子分别命名为IL-17、V11-17和IL-17R。
Herpesvirus Saimiri gene 13 (HVS13) exhibits 57% identity with the predicted sequence of a T cell-derived molecule termed CTLA8. Recombinant HVS13 and CTLA8 stimulate transcriptional factor NF-kappa B activity and interleukin-6 (IL-6) secretion in fibroblasts, and costimulate T cell proliferation. An HVS13.Fc fusion protein was used to isolate a cDNA encoding a novel receptor that also binds CTLA8. This receptor is unrelated to previously identified cytokine receptor families. A recombinant soluble receptor inhibited T cell proliferation and IL-2 production induced by PHA, concanavalin A (conA), and anti-TCR MAb. These results define CTLA8 and HVS13 as novel cytokines that bind to a novel cytokine receptor. We propose to call these molecules IL-17, vlL-17, and IL-17R, respectively.