Article
Hypomorphic MGAT5 polymorphisms promote multiple sclerosis cooperatively with MGAT1 and interleukin-2 and 7 receptor variants.
Journal of neuroimmunology - 15 Mar 2013
Li Carey F, Zhou Raymond W, Mkhikian Haik, Newton Barbara L, Yu Zhaoxia, Demetriou Michael
Abstract excerpt
Deficiency of the Golgi N-glycan branching enzyme Mgat5 in mice promotes T cell hyperactivity, endocytosis of CTLA-4 and autoimmunity, including a spontaneous multiple sclerosis (MS)-like disease. Multiple genetic and environmental MS risk factors lower N-glycan branching in T cells. These include variants in interleukin-2 receptor-α (IL2RA), interleukin-7 receptor-α (IL7RA), and MGAT1, a Golgi branching enzyme...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.