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抗Pgp-1(CD44)抗体对超抗原诱导的T细胞缺失的调节作用

Modulation of superantigen-induced T-cell deletion by antibody anti-Pgp-1 (CD44).

作者信息

Ayroldi E, Cannarile L, Ricardi C

机构信息

Department of Clinical Medicine, Pathology and Pharmacology, Perugia University Medical School, Italy.

出版信息

Immunology. 1996 Feb;87(2):191-7. doi: 10.1046/j.1365-2567.1996.466540.x.

Abstract

We examined the effects of anti-Pgp-1 (CD44) antibody on the in vitro deletion of murine CD4 and CD8 single positive T cells induced by Staphylococcal enterotoxin B (SEB). Soluble anti-Pgp-1 antibody enhanced the apoptosis and decreased the proliferation of SEB-responding T cells. In contrast, cross-linked anti-Pgp-1 antibody provided costimulatory signals for the T-cell activation induced by anti-CD3 antibody. Hyaluronic acid (HA), a ligand of Pgp-1, did not affect proliferation and deletion induced by SEB, whereas it mimicked the effects of the cross-linked antibody in anti-CD3-driven proliferation. T-cell Pgp-1 surface expression after 48 hr incubation with SEB was unchanged as compared to unstimulated cells. However, when the memory T cells were established, some V beta 8+ (SEB-specific) T cells Pgp-1low became Pgp-1high, displaying a bimodal character. Moreover, the Pgp-1 increased expression correlated with an increase of Pgp-1 soluble form in the supernatant. These findings suggested that signals following the triggering of the Pgp-1 molecule are important in controlling T-cell survival.

摘要

我们研究了抗Pgp-1(CD44)抗体对葡萄球菌肠毒素B(SEB)诱导的小鼠CD4和CD8单阳性T细胞体外缺失的影响。可溶性抗Pgp-1抗体增强了SEB反应性T细胞的凋亡并降低了其增殖。相反,交联的抗Pgp-1抗体为抗CD3抗体诱导的T细胞活化提供了共刺激信号。透明质酸(HA),Pgp-1的一种配体,不影响SEB诱导的增殖和缺失,而它在抗CD3驱动的增殖中模拟了交联抗体的作用。与未刺激的细胞相比,与SEB孵育48小时后T细胞Pgp-1的表面表达没有变化。然而,当建立记忆T细胞时,一些Vβ8 +(SEB特异性)T细胞Pgp-1低水平变为Pgp-1高水平,呈现双峰特征。此外,Pgp-1表达增加与上清液中Pgp-1可溶性形式的增加相关。这些发现表明,Pgp-1分子触发后的信号在控制T细胞存活中很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eb6/1384273/bb626fef3134/immunology00059-0027-a.jpg

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