Store-Operated Calcium Entry Controls Innate and Adaptive Immune Cell Function in Inflammatory Bowel Disease

T cell-specific deletion of CRAC channel genes in mice showed that Orai1, Stim1, and Stim2-deficient T cells had quantitatively distinct defects in store-operated Ca2+ entry , which correlated with gradually more pronounced impairment of cytokine production by Th1 and Th17 cells and the severity of inflammatory bowel disease.