title: Kv1.3 channels as a potential target for immunomodulation of CD4+ CD28null T cells in patients with acute coronary syndrome.
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(+)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.
authors.affiliation: Department of Gerontology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Rende
authors.initials: R
authors.lastname: Xu
authors.forename: Ming
authors.initials: M
authors.lastname: Cao
authors.forename: Xiaofen
authors.initials: X
authors.lastname: Wu
authors.forename: Xingfen
authors.initials: X
authors.lastname: Wang
authors.forename: Lei
authors.initials: L
authors.lastname: Ruan
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Quan
authors.forename: Caixia
authors.initials: C
authors.lastname: Lü
authors.forename: Wei
authors.initials: W
authors.lastname: He
authors.forename: Cuntai
authors.initials: C
authors.lastname: Zhang
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000276:immunology / Q000378:metabolism; D000368:Aged; D018106:CD28 Antigens / Q000378:metabolism*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D016022:Case-Control Studies; D005260:Female; D005363:Ficusin / Q000494:pharmacology; D006801:Humans; D056747:Immunomodulation; D007371:Interferon-gamma / Q000037:antagonists & inhibitors / Q000378:metabolism; D051664:Kv1.3 Potassium Channel / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D000073718:Pancreatitis-Associated Proteins; D054353:Perforin / Q000037:antagonists & inhibitors / Q000378:metabolism; D024681:Potassium Channels, Calcium-Activated / Q000276:immunology / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism*
chemical_list: C499898:5-(4-phenylbutoxy)psoralen; D018106:CD28 Antigens; D051664:Kv1.3 Potassium Channel; D000073718:Pancreatitis-Associated Proteins; D024681:Potassium Channels, Calcium-Activated; C000612141:REG3A protein, human; D054353:Perforin; D007371:Interferon-gamma; D005363:Ficusin