Kv1.3 channels as a potential target for immunomodulation of CD4+CD28null T cells in patients with acute coronary syndrome

被引：19

作者：

Xu, Rende ^{[1
]}

Cao, Ming ^{[1
]}

Wu, Xiaofen ^{[1
]}

Wang, Xingfen ^{[1
]}

Ruan, Lei ^{[1
]}

Quan, Xiaoqing ^{[1
]}

Lii, Caixia ^{[1
]}

He, Wei ^{[1
]}

Zhang, Cuntai ^{[1
]}

机构：

[1] Huazhong Univ Sci & Technol, Dept Gerontol, Tongji Hosp, Tongji Med Coll, Wuhan 430030, Peoples R China

来源：

CLINICAL IMMUNOLOGY | 2012年 / 142卷 / 02期

基金：

中国国家自然科学基金;

关键词：

Acute coronary syndrome; CD4(+)CD28(null) T cell; K+ channel; POTASSIUM CHANNEL; AUTOIMMUNE-DISEASES; MULTIPLE-SCLEROSIS; K+ CHANNELS; LYMPHOCYTE; COSTIMULATION; SUPPRESSION; EXPRESSION; BLOCKADE;

D O I：

10.1016/j.clim.2011.10.009

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Modulation of CD4(+)CD28(null) T cells through K. channels could provide potential novel targets for the treatment acute coronary syndrome (ACS). However, the surface phenotype and K+ channel expression of CD4(+)CD28(null) T cells in patients with ACS is unclear. The aim of this study was to investigate the surface phenotype and K+ channel expression of CD4(+)CD28(null) T cells in patients with ACS. We found that more than 80% of CD4(+)CD28(null) T cells in patients with ACS showed a CD45RA(-)CD45RO(+)CCR7(-) surface phenotype. CD4(+)CD28(null) T expressed small numbers of the voltage-gated Kv1.3 and intermediate-conductance Ca2+-activated K+ channel KCa3.1 when quiescent, but increased Kv1.3 expression 4-fold with little change in KCa3.1 levels upon activation. Consistent with their channel phenotypes, the production of interferon-gamma and perforin in CD4(+)CD28(null) T cells was suppressed by the specific Kv1.3 blocker 5-(4-phenoxybutoxy)psoralen PAP-1. Therefore, selective targeting of Kv1.3 in CD4(+)CD28(null) T cells may hold potential therapeutic promise for ACS. (C) 2011 Elsevier Inc. All rights reserved.

引用

页码：209 / 217

页数：9

共 25 条

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