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In lymphoid and myeloid cells, membrane hyperpolarization by the opening of K + channels increases the activity of Ca 2+ release-activated Ca 2+ (CRAC) channels and transient receptor potential (TRP) Ca 2+ channels. The intermediate-conductance Ca 2+ -activated K + channel K Ca 3.1 plays an important role in cell proliferation, differentiation, migration, and cytokine production in innate and adaptive immune systems. K Ca 3.1 is therefore an attractive therapeutic target for allergic, inflammatory, and autoimmune disorders. In the past several years, studies have provided new insights into 1) K Ca 3.1 pharmacology and its auxiliary regulators; 2) post-transcriptional and proteasomal regulation of K Ca 3.1; 3) K Ca 3.1 as a regulator of immune cell migration, cytokine production, and phenotypic polarization; 4) the role of K Ca 3.1 in the phosphorylation and nuclear translocation of Smad2/3; and 5) K Ca 3.1 as a therapeutic target for cancer immunotherapy. In this review, we have assembled a comprehensive overview of current research on the physiological and pathophysiological significance of K Ca 3.1 in the immune system.

Ca<sup>2+</sup>-Activated K<sup>+</sup> Channel K<sub>Ca</sub>3.1 as a Therapeutic Target for Immune Disorders