Interleukin 21 Drives a Hypermetabolic State and CD4+ T-Cell–Associated Pathogenicity in Chronic Intestinal Inflammation
Interleukin 21 induces metabolic alterations and acquisition of an inflammatory-like phenotype by perturbing mitochondria–endoplasmic reticulum crosstalk, thereby diminishing the capacity of Tregs in suppressing inflammatory bowel disease.
