FOXP3+Treg Cell Stability and its role in Immunometabolism Sep. 21 (WED) 11:00 / Auditorium (1F), PBC Bin Li Institute Pasteur of Shanghai, CAS Increasing evidences reveal the alterations of glucose, lipid and amino acid metabolism of T cells upon activation, indicating the metabolic reprogramming of T cells is an important hallmark of activation. FOXP3+ regulatory T cells (Treg) play a critical role in the maintenance of immune tolerance. The immunosuppressive phenotype of Tregs is largely determined by the gene expression patterns resulting from the action of FOXP3 and its cooperation with a number of transcriptional co-regulator factors. The molecular mechanism underlying FOXP3+ Treg mediated immune suppression includes cell-cell contact dependent and independent molecular events such as immunometabolic regulation, but still remains largely unclear. Work from our group, and a growing number of others, has demonstrated that, in addition to transcriptional control of the FOXP3 gene, expression and function of this important transcription factor is determined by mechanisms active at the posttranslational level. Moreover, these pathways of FOXP3 regulation significantly impact the in vitro and in vivo function of Treg cells. I will discuss more recent progress related to tissue Treg cell stability in vivo and its role in immunometabolic regulation during the lecture. Inquiry: Dr. Dipayan Rudra (279-9865) or AIM Administrative Team (Tel.279-8628, E-mail: varsha@ibs.re.kr)