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10.1038/ncomms14644

http://scihub22266oqcxt.onion/10.1038/ncomms14644
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suck abstract from ncbi


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pmid28248292
      Nat+Commun 2017 ; 8 (ä): 14644
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  • Potassium channels Kv1 3 and KCa3 1 cooperatively and compensatorily regulate antigen-specific memory T cell functions #MMPMID28248292
  • Chiang EY ; Li T ; Jeet S ; Peng I ; Zhang J ; Lee WP ; DeVoss J ; Caplazi P ; Chen J ; Warming S ; Hackos DH ; Mukund S ; Koth CM ; Grogan JL
  • Nat Commun 2017[Mar]; 8 (ä): 14644 PMID28248292 show ga
  • Voltage-gated Kv1.3 and Ca(2+)-dependent KCa3.1 are the most prevalent K(+) channels expressed by human and rat T cells. Despite the preferential upregulation of Kv1.3 over KCa3.1 on autoantigen-experienced effector memory T cells, whether Kv1.3 is required for their induction and function is unclear. Here we show, using Kv1.3-deficient rats, that Kv1.3 is involved in the development of chronically activated antigen-specific T cells. Several immune responses are normal in Kv1.3 knockout (KO) rats, suggesting that KCa3.1 can compensate for the absence of Kv1.3 under these specific settings. However, experiments with Kv1.3 KO rats and Kv1.3 siRNA knockdown or channel-specific inhibition of human T cells show that maximal T-cell responses against autoantigen or repeated tetanus toxoid stimulations require both Kv1.3 and KCa3.1. Finally, our data also suggest that T-cell dependency on Kv1.3 or KCa3.1 might be irreversibly modulated by antigen exposure.
  • |*Immunologic Memory/drug effects [MESH]
  • |Animals [MESH]
  • |Epitopes/*immunology [MESH]
  • |Gene Knockdown Techniques [MESH]
  • |Humans [MESH]
  • |Immunity/drug effects [MESH]
  • |Intermediate-Conductance Calcium-Activated Potassium Channels/deficiency/*metabolism [MESH]
  • |Kv1.3 Potassium Channel/*metabolism [MESH]
  • |Lymphocyte Activation/immunology [MESH]
  • |Phenotype [MESH]
  • |Potassium Channel Blockers/pharmacology [MESH]
  • |RNA, Small Interfering/metabolism [MESH]
  • |Rats [MESH]


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