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231224s2012 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2011.10.009
|2 doi
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|a pubmed24n0713.xml
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|a (DE-627)NLM213858827
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|a (NLM)22169811
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Xu, Rende
|e verfasserin
|4 aut
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|a Kv1.3 channels as a potential target for immunomodulation of CD4+ CD28null T cells in patients with acute coronary syndrome
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|c 2012
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 11.04.2012
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|a Date Revised 16.11.2017
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|a published: Print-Electronic
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|a CommentIn: Clin Immunol. 2012 Feb;142(2):105-6. - PMID 22189042
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|a Citation Status MEDLINE
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|a Copyright © 2011 Elsevier Inc. All rights reserved.
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|a 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
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a 5-(4-phenylbutoxy)psoralen
|2 NLM
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|a CD28 Antigens
|2 NLM
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|a Kv1.3 Potassium Channel
|2 NLM
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|a Pancreatitis-Associated Proteins
|2 NLM
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|a Potassium Channels, Calcium-Activated
|2 NLM
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|a REG3A protein, human
|2 NLM
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|a Perforin
|2 NLM
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|a 126465-35-8
|2 NLM
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|a Interferon-gamma
|2 NLM
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|a 82115-62-6
|2 NLM
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|a Ficusin
|2 NLM
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|a KTZ7ZCN2EX
|2 NLM
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|a Cao, Ming
|e verfasserin
|4 aut
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|a Wu, Xiaofen
|e verfasserin
|4 aut
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|a Wang, Xingfen
|e verfasserin
|4 aut
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|a Ruan, Lei
|e verfasserin
|4 aut
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|a Quan, Xiaoqing
|e verfasserin
|4 aut
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|a Lü, Caixia
|e verfasserin
|4 aut
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|a He, Wei
|e verfasserin
|4 aut
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|a Zhang, Cuntai
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 142(2012), 2 vom: 14. Feb., Seite 209-17
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:142
|g year:2012
|g number:2
|g day:14
|g month:02
|g pages:209-17
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|u http://dx.doi.org/10.1016/j.clim.2011.10.009
|3 Volltext
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|a AR
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|d 142
|j 2012
|e 2
|b 14
|c 02
|h 209-17
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