Blockade of Ca2+-activated K+ channels in T cells: an option for the treatment of multiple sclerosis?
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Blockade of Ca2+-activated K+ channels in T cells: an option for the treatment of multiple sclerosis? / Madsen, Lars Siim; Christophersen, Palle; Olesen, Søren-Peter.
In: European Journal of Immunology, Vol. 35, No. 4, 2005, p. 1023-6.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Blockade of Ca2+-activated K+ channels in T cells: an option for the treatment of multiple sclerosis?
AU - Madsen, Lars Siim
AU - Christophersen, Palle
AU - Olesen, Søren-Peter
N1 - Keywords: Animals; Mice; Multiple Sclerosis; Potassium Channels, Calcium-Activated; T-Lymphocytes
PY - 2005
Y1 - 2005
N2 - Voltage- and Ca(2+)-dependent K(+) channels in the membrane of both T and B lymphocytes are important for the cellular immune response. In the current issue of the European Journal of Immunology, Reich et al. demonstrate that selective blockade of the intermediate-conductance Ca(2+)-activated K(+) channel (the IK channel encoded by the KCNN4 gene) prevents cytokine production in the spinal chord and ameliorates the development of EAE caused by injection of myelin oligodendrocyte glycoprotein (MOG)(35-55) in mice. These data renew the focus on the IK channel as a potential target for the development of new immune-suppressant drugs for the treatment of autoimmune diseases.
AB - Voltage- and Ca(2+)-dependent K(+) channels in the membrane of both T and B lymphocytes are important for the cellular immune response. In the current issue of the European Journal of Immunology, Reich et al. demonstrate that selective blockade of the intermediate-conductance Ca(2+)-activated K(+) channel (the IK channel encoded by the KCNN4 gene) prevents cytokine production in the spinal chord and ameliorates the development of EAE caused by injection of myelin oligodendrocyte glycoprotein (MOG)(35-55) in mice. These data renew the focus on the IK channel as a potential target for the development of new immune-suppressant drugs for the treatment of autoimmune diseases.
U2 - 10.1002/eji.200526078
DO - 10.1002/eji.200526078
M3 - Journal article
C2 - 15770695
VL - 35
SP - 1023
EP - 1026
JO - European Journal of Immunology
JF - European Journal of Immunology
SN - 0014-2980
IS - 4
ER -
ID: 8466454