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CD58与CD2反受体之间的分子相互作用介导了单核细胞通过白细胞介素-12增强T细胞活化的能力。

Molecular interaction between CD58 and CD2 counter-receptors mediates the ability of monocytes to augment T cell activation by IL-12.

作者信息

Gollob J A, Li J, Kawasaki H, Daley J F, Groves C, Reinherz E L, Ritz J

机构信息

Laboratory of Immunobiology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.

出版信息

J Immunol. 1996 Sep 1;157(5):1886-93.

PMID:8757306
Abstract

IL-12 stimulates both T and NK cells and is pivotal in the development of the Th1 immune response. In this work, we show that an interaction between CD2 and CD58 on activated T cells and monocytes, respectively, regulates the T cell response to IL-12. B cells provide little IL-12-specific costimulation, and this correlates with the low level of CD58 on B cells relative to monocytes and the lack of significant up-regulation in response to IFN-gamma or PHA activation. CHO cell transfectants expressing CD58 at a level comparable with that found on monocytes restore IL-12 responsiveness to APC-depleted T cells. This effect is not observed with CHO cells expressing CD48, a second CD2 ligand with a low avidity for CD2 relative to CD58. Thus, in addition to augmenting adhesion between T cells and their cognate APCs and facilitating TCR-triggered activation, the CD2-CD58 interaction uniquely optimizes the T cell response to IL-12.

摘要

白细胞介素-12刺激T细胞和自然杀伤细胞,在Th1免疫反应的发展中起关键作用。在本研究中,我们发现活化的T细胞和单核细胞上的CD2与CD58之间的相互作用分别调节T细胞对白细胞介素-12的反应。B细胞几乎不提供白细胞介素-12特异性共刺激,这与B细胞上CD58水平相对于单核细胞较低以及对干扰素-γ或PHA激活缺乏显著上调有关。表达与单核细胞上水平相当的CD58的CHO细胞转染体恢复了APC缺陷型T细胞对白细胞介素-12的反应性。相对于CD58对CD2亲和力较低的第二种CD2配体CD48的CHO细胞未观察到这种效应。因此,除了增强T细胞与其同源抗原呈递细胞之间的黏附并促进TCR触发的激活外,CD2-CD58相互作用独特地优化了T细胞对白细胞介素-12的反应。

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