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

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.

► Most of CD4+CD28null T cells in ACS patient showed a CD45RA-CD45RO+CCR7- phenotype. ► The majority of CD4+CD28null T cells from ACS are Kv1.3highKCa3.1low T cells. ► The actions of CD4+CD28null T cells was reduced by Kv1.3 blockers like PAP-1.