Mathematics Faculty Articles
GDP-L-Fucose Synthase is a CD4+ T Cell–Specific Autoantigen in DRB3*02:02 Patients with Multiple Sclerosis
Document Type
Article
Publication Date
10-10-2018
Publication Title
Science Translational Medicine
ISSN
1946-6234
Volume
10
Issue/No.
462
First Page
eaat4301
Abstract
Multiple sclerosis is an immune-mediated autoimmune disease of the central nervous system that develops in genetically susceptible individuals and likely requires environmental triggers. The autoantigens and molecular mimics triggering the autoimmune response in multiple sclerosis remain incompletely understood. By using a brain-infiltrating CD4+ T cell clone that is clonally expanded in multiple sclerosis brain lesions and a systematic approach for the identification of its target antigens, positional scanning peptide libraries in combination with biometrical analysis, we have identified guanosine diphosphate (GDP)–L-fucose synthase as an autoantigen that is recognized by cerebrospinal fluid–infiltrating CD4+ T cells from HLA-DRB3*–positive patients. Significant associations were found between reactivity to GDP-L-fucose synthase peptides and DRB3*02:02 expression, along with reactivity against an immunodominant myelin basic protein peptide. These results, coupled with the cross-recognition of homologous peptides from gut microbiota, suggest a possible role of this antigen as an inducer or driver of pathogenic autoimmune responses in multiple sclerosis.
Additional Comments
DFG Center grant #s: SFB 841, SNF: 310030_146945; European Research Council Advanced Grant #: 340733
NSUWorks Citation
Planas, Raquel; Santos, Radleigh; Tomas-Ojer, Paula; Cruciani, Carolina; Lutterotti, Andreas; Faigle, Wolfgang; Schaeren-Wiemers, Nicole; Espejo, Carmen; Eixarch, Herena; Pinilla, Clemencia; Martin, Roland; and Sospedra, Mireia, "GDP-L-Fucose Synthase is a CD4+ T Cell–Specific Autoantigen in DRB3*02:02 Patients with Multiple Sclerosis" (2018). Mathematics Faculty Articles. 284.
https://nsuworks.nova.edu/math_facarticles/284
DOI
10.1126/scitranslmed.aat4301
Comments
©2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works