Ca2+-Activated K+ Channel KCa3.1 Regulates Il-10 Expression in Regulatory T Cells at the Recovery Phase of Inflammatory Bowel Disease Model

Abstract

Inflammatory bowel diseases (IBD) are chronic inflammatory diseases of the gastrointestinal tract, arising from abnormal responses of the innate and adaptative immune system. Interleukin-10 (IL-10)-producing regulatory T (Treg) cells play a protective role at the recovery phase of IBD. Here, effects of subcutaneous administration of the selective KCa3.1 inhibitor TRAM-34 on disease activities were explored in chemically-induced, semi-chronic IBD (scIBD) model mice. The administration of 1 mg/kg TRAM-34 elicited a significant decrease in IBD disease severity, compared with vehicle-administrated mice.