Author/Authors :
Xu، نويسنده , , Rende and Cao، نويسنده , , Ming and Wu، نويسنده , , Xiaofen and Wang، نويسنده , , Xingfen and Ruan، نويسنده , , Xin Gen Lei and Quan Hao، نويسنده , , Xiaoqing and Lu، نويسنده , , Caixia and He، نويسنده , , Wei and Zhang، نويسنده , , Cuntai، نويسنده ,
Abstract :
Modulation of CD4+CD28null 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+CD28null 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+CD28null T cells in patients with ACS. We found that more than 80% of CD4+CD28null T cells in patients with ACS showed a CD45RA−CD45RO+CCR7− surface phenotype. CD4+CD28null 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-γ and perforin in CD4+CD28null T cells was suppressed by the specific Kv1.3 blocker 5-(4-phenoxybutoxy)psoralen PAP-1. Therefore, selective targeting of Kv1.3 in CD4+CD28null T cells may hold potential therapeutic promise for ACS.
