CARMA1、Bcl10和MALT1在抗原受体信号传导中的作用。

The roles of CARMA1, Bcl10, and MALT1 in antigen receptor signaling.

作者信息

Lin Xin, Wang Demin

机构信息

Department of Microbiology and Immunology, University at Buffalo, 138 Farber Hall, 3435 Main Street, Buffalo, NY 14214, USA.

出版信息

Semin Immunol. 2004 Dec;16(6):429-35. doi: 10.1016/j.smim.2004.08.022.

DOI:10.1016/j.smim.2004.08.022

PMID:15541657

Abstract

Lymphocyte activation plays a critical role in immune responses. Dysregulation of lymphocyte activation can cause autoimmune, immunodeficient diseases, or leukemia/lymphoma. Lymphocyte activation is triggered by stimulation of antigen receptors, T cell receptors (TCR) or B cell receptors (BCR), on the surfaces of T or B lymphocyte, respectively. Stimulation of TCR or BCR induces a series of signal transduction cascades leading to activation of multiple transcription factors including NF-kappaB. Recent studies demonstrate that CARMA1, a scaffold protein, plays an essential role in mediating TCR- or BCR-induced NF-kappaB activation by recruiting two adaptor proteins, Bcl10 and MALT1, to lipid rafts following stimulation of antigen receptors. In this review, we will discuss the mechanism by which proximal signaling components connect antigen receptor signaling to CARMA1, and how CARMA1 regulates Bcl10 and MALT1, leading to activation of NF-kappaB. In addition, the roles of CARMA1, Bcl10, and MALT1 in lymphocyte activation and development will also be discussed.

摘要

淋巴细胞活化在免疫反应中起关键作用。淋巴细胞活化失调可导致自身免疫性疾病、免疫缺陷疾病或白血病/淋巴瘤。淋巴细胞活化分别由T淋巴细胞或B淋巴细胞表面的抗原受体、T细胞受体（TCR）或B细胞受体（BCR）的刺激所触发。TCR或BCR的刺激诱导一系列信号转导级联反应，导致包括NF-κB在内的多种转录因子活化。最近的研究表明，支架蛋白CARMA1在抗原受体刺激后通过将两种衔接蛋白Bcl10和MALT1募集到脂筏中，在介导TCR或BCR诱导的NF-κB活化中起重要作用。在本综述中，我们将讨论近端信号成分将抗原受体信号与CARMA1连接的机制，以及CARMA1如何调节Bcl10和MALT1，从而导致NF-κB活化。此外，还将讨论CARMA1、Bcl10和MALT1在淋巴细胞活化和发育中的作用。