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松鼠猴疱疹病毒编码一种新的细胞因子IL-17,它可与一种新型细胞因子受体结合。

Herpesvirus Saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor.

作者信息

Yao Z, Fanslow W C, Seldin M F, Rousseau A M, Painter S L, Comeau M R, Cohen J I, Spriggs M K

机构信息

Immunex Corporation, Seattle, Washington 98101, USA.

出版信息

Immunity. 1995 Dec;3(6):811-21. doi: 10.1016/1074-7613(95)90070-5.

Abstract

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, vIL-17, and IL-17R, respectively.

摘要

松鼠猴疱疹病毒基因13(HVS13)与一种名为CTLA8的T细胞衍生分子的预测序列具有57%的同一性。重组HVS13和CTLA8可刺激成纤维细胞中的转录因子NF-κB活性和白细胞介素-6(IL-6)分泌,并共同刺激T细胞增殖。一种HVS13.Fc融合蛋白被用于分离编码一种也能结合CTLA8的新型受体的cDNA。该受体与先前鉴定的细胞因子受体家族无关。一种重组可溶性受体抑制了由PHA、刀豆球蛋白A(ConA)和抗TCR单克隆抗体诱导的T细胞增殖和IL-2产生。这些结果将CTLA8和HVS13定义为与新型细胞因子受体结合的新型细胞因子。我们建议分别将这些分子称为IL-17、vIL-17和IL-17R。

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