biostudies-literatureUnknown48(11)Jeong EMTransglutaminase 2 (TG2) is a ubiquitously expressed enzyme that catalyzes crosslinking, polyamination or deamidation of glutamine residues in proteins. It has been reported that TG2 is involved in the pathogenesis of various inflammatory diseases including celiac disease, pulmonary fibrosis, cystic fibrosis, multiple sclerosis and sepsis. Recently, using a mouse model of bleomycin-induced lung fibrosis, we showed that TG2 is required to trigger inflammation via the induction of T helper type 17 (Th17) cell differentiation in response to tissue damage. However, the role of TG2 in inflammatory bowel disease (IBD), which is thought to be a Th17 cell-associated disease, has remained elusive. In this study, we investigated the role of TG2 in dextran sulfate sodium (DSS)-induced colitis, the moExperimental & molecular medicinee267https://www.ebi.ac.uk/biostudies/studies/S-EPMC5133373biostudies-literatureTransglutaminase 2 is dispensable but required for the survival of mice in dextran sulfate sodium-induced colitis.PMC5133373Jeong EMChoi YKim JHKim IGSon YHCho SYLee JHfalseTransglutaminase 2 is dispensable but required for the survival of mice in dextran sulfate sodium-induced colitis.Transglutaminase 2 (TG2) is a ubiquitously expressed enzyme that catalyzes crosslinking, polyamination or deamidation of glutamine residues in proteins. It has been reported that TG2 is involved in the pathogenesis of various inflammatory diseases including celiac disease, pulmonary fibrosis, cystic fibrosis, multiple sclerosis and sepsis. Recently, using a mouse model of bleomycin-induced lung fibrosis, we showed that TG2 is required to trigger inflammation via the induction of T helper type 17 (Th17) cell differentiation in response to tissue damage. However, the role of TG2 in inflammatory bowel disease (IBD), which is thought to be a Th17 cell-associated disease, has remained elusive. In this study, we investigated the role of TG2 in dextran sulfate sodium (DSS)-induced colitis, the mo2016-01-01T00:00:00Z2016 Nov2025-06-01T01:09:25.812Z2025-06-01T01:09:25.812ZS-EPMC51333732781193610.1038/emm.2016.95