| Title | Dysregulation of T cell receptor N-glycosylation: A molecular mechanism involved in ulcerative colitis |
| Publication Type | Journal Article |
| 2014 |
| Authors | Dias, AM, Dourado, J, Lago, P, Cabral, J, Marcos-Pinto, R, Salgueiro, P, Almeida, CR, Carvalho, S, Fonseca, S, Lima, M, Vilanova, M, Dinis-Ribeiro, M, Reis, CA, Pinho, SS |
| Journal | Human Molecular Genetics |
| Volume | 23 |
| Issue | 9 |
| Pagination | 2416 - 2427 |
| Date Published | 2014 |
| The incidence of inflammatory bowel disease is increasing worldwide and the underlying molecular mechanisms are far from being fully elucidated. Herein, we evaluated the role of N-glycosylation dysregulation in T cells as a key mechanism in the ulcerative colitis (UC) pathogenesis. The evaluation of the branched N-glycosylation levelsandprofile of intestinalTcell receptor (TCR)wereassessedin colonic biopsies fromUCpatientsand healthy controls. Expression alterations of the glycosyltransferase gene MGAT5 were also evaluated. We demonstrated thatUCpatients exhibit a dysregulation ofTCRbranchedN-glycosylationonlamina propriaTlymphocytes. Patients with severe UC showed the most pronounced defect on N-glycan branching in T cells. Moreover, UC patients showed a significant reduction of MGAT5 gene transcription in T lymphocytes. In this study, we disclose for the first time that a deficiency in branched N-glycosylation on TCR due to a reduced MGAT5 gene expression is a new molecular mechanism underlying UC pathogenesis, being a potential novel biomarker with promising clinical and therapeutic applications. © The Author 2013. Published by Oxford University Press. All rights reserved. |
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