5-(4-phenylbutoxy)psoralen and 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(+)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-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.

Topics: Acute Coronary Syndrome; Aged; Case-Control Studies; CD28 Antigens; CD4-Positive T-Lymphocytes; Female; Ficusin; Humans; Immunomodulation; Interferon-gamma; Kv1.3 Potassium Channel; Male; Middle Aged; Pancreatitis-Associated Proteins; Perforin; Potassium Channels, Calcium-Activated; T-Lymphocyte Subsets