T cell activation and function depend on Ca signals mediated by store-operated Ca entry (SOCE) through Ca release-activated Ca (CRAC) channels formed by ORAI1 proteins. We here investigated how SOCE controls T cell function in pulmonary inflammation during a T helper 1 (T1) cell-mediated response to influenza A virus (IAV) infection and T2 cell-mediated allergic airway inflammation. T cell-specific deletion of did not exacerbate pulmonary inflammation and viral burdens following IAV infection but protected mice from house dust mite-induced allergic airway inflammation.
View Article and Find Full Text PDFInflammatory bowel disease (IBD) is characterized by dysregulated intestinal immune responses. Using mass cytometry (CyTOF) to analyze the immune cell composition in the lamina propria (LP) of patients with ulcerative colitis (UC) and Crohn's disease (CD), we observed an enrichment of CD4 effector T cells producing IL-17A and TNF, CD8 T cells producing IFNγ, T regulatory (Treg) cells, and innate lymphoid cells (ILC). The function of these immune cells is regulated by store-operated Ca entry (SOCE), which results from the opening of Ca release-activated Ca (CRAC) channels formed by ORAI and STIM proteins.
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