Abstract

Two-pore domain potassium channels, such as TASK, are essential players in the regulation of the resting membrane potential. A recent publication in Experimental Neurology revealed that the pharmacological blockade of the two-pore domain potassium channel TASK1 improved clinical disease severity, the number of cellular infiltrates, as well as the degree of demyelination in experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis. This effect was driven by a reduction in the generation of proinflammatory cytokines and proliferation of T lymphocytes. Thus, functional activity of T lymphocytes was identified to be TASK1 dependent suggesting that this class of potassium channels may represent an interesting target for treating T cell-driven autoimmunity directed against the central nervous system.

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