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SummaryBackground. The Kv1.3 voltage-gated potassium channel is selectively upregulated upon activation in effector memory T (T EM ) cells in inflamed tissue, and plays an important role in maintenance of T-cell activation. Although Kv1.3 blockers have been shown to ameliorate allergic contact dermatitis (ACD) in a rat model, it remains unknown whether the effect of Kv1.3 blockers on ACD is mediated by suppressing T EM cell function and/or whether naive T-cells or central memory T (T CM ) cells are influenced. Aim. To analyse the detailed mechanism of Kv1.3 blockers in a rat model of ACD. Methods. We examined the effects of a Kv1.3 blocker on inflammation and production of the effector cytokine interferon (IFN)-c in inflamed tissue in rat ACD. Singlecell suspensions were isolated from inflamed rat ears (T EM cells), and regional lymph nodes (naive T/T CM cells), and the effect of Kv1.3 blockers on anti-CD3-stimulated IFN-c production in vitro was measured.Results. The Kv1.3 blocker significantly suppressed ear inflammation and IFN-c production at the protein level in vivo. It also suppressed in vitro IFN-c production from T EM cells from inflamed tissues, but did not suppress the function of naive T/T CM cells from lymph nodes. Conclusions. We found that the Kv1.3 blocker ameliorated ACD by inhibiting T EM cell functions only, thus Kv1.3 blockers could be a potentially selective therapeutic agent for T EM cell-mediated inflammatory skin diseases without producing harmful side-effects.