Summary Background The Kv1.3 voltage‐gated potassium channel is selectively upregulated upon activation in effector memory T (TEM) 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 TEM cell function and/or whether naive T‐cells or central memory T (TCM) 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)‐γ in inflamed tissue in rat ACD. Single‐cell suspensions were isolated from inflamed rat ears (TEM cells), and regional lymph nodes (naive T/TCM cells), and the effect of Kv1.3 blockers on anti‐CD3‐stimulated IFN‐γ production in vitro was measured. Results The Kv1.3 blocker significantly suppressed ear inflammation and IFN‐γ production at the protein level in vivo. It also suppressed in vitro IFN‐γ production from TEM cells from inflamed tissues, but did not suppress the function of naive T/TCM cells from lymph nodes. Conclusions We found that the Kv1.3 blocker ameliorated ACD by inhibiting TEM cell functions only, thus Kv1.3 blockers could be a potentially selective therapeutic agent for TEM cell‐mediated inflammatory skin diseases without producing harmful side‐effects. Click here for the corresponding questions to this CME article.