Heikrujam Thoihen Meitei, Neeraja Kulkarni, Amey Shirolkar, Srikanth Rapole, Praveen Sharma, Vikkarasan Rehman Mujeeb, Sharad Srivastava, Girdhari Lal
) during colitis. This signaling induces the rapamycin-sensitive phosphorylation of PI3K, Akt, mTORC1, and STAT3 in a CCR6-dependent manner. RNA-seq and proteomics analysis revealed that the addition of CCL20 during Th17 differentiation affects several metabolic pathways, including energy metabolism. CCL20 significantly increased glycolysis and inhibited oxidative phosphorylation, thereby driving the differentiation of pathogenic Th17 cells. Our findings suggest that alterations in CCR6-induced changes in Th17 metabolism offer an interesting therapeutic target for gut inflammation and autoimmunity.