Calcium Signaling Controls Pathogenic Th17 Cell-Mediated Inflammation by Regulating Mitochondrial Function (Cell Metabolism)

Kaufmann et al. show an essential role of the store-operated calcium item (SOCE) pathway in pathogenic Th17 cell function by regulating mitochondrial function and OXPHOS, and preventing oxidative stress. SOCE inhibition could be a potential therapeutic avenue in Th17 inflammatory diseases such as MS, colitis, psoriasis, or steroid-resistant asthma.