scholarly journals Mnk1 and 2 Are Dispensable for T Cell Development and Activation but Important for the Pathogenesis of Experimental Autoimmune Encephalomyelitis

2012 ◽  
Vol 190 (3) ◽  
pp. 1026-1037 ◽  
Author(s):  
Balachandra K. Gorentla ◽  
Sruti Krishna ◽  
Jinwook Shin ◽  
Makoto Inoue ◽  
Mari L. Shinohara ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
T Cell Development ◽  
Cell Development ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals Mgat5 Deficiency in T Cells and Experimental Autoimmune Encephalomyelitis

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Ani Grigorian ◽  
Michael Demetriou
Keyword(s):  
T Cells ◽  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Demyelinating Disease ◽  
Cell Receptor ◽  
Protein Glycosylation ◽  
Autoimmune Encephalomyelitis ◽  
Glycosylation Pathway ◽  
Experimental Autoimmune ◽  
Surface Glycoproteins

Multiple sclerosis (MS) is an inflammatory demyelinating and neurodegenerative disease initiated by autoreactive T cells. Mgat5, a gene in the Asn (N-) linked protein glycosylation pathway, associates with MS severity and negatively regulates experimental autoimmune encephalomyelitis (EAE) and spontaneous inflammatory demyelination in mice. N-glycan branching by Mgat5 regulates interaction of surface glycoproteins with galectins, forming a molecular lattice that differentially controls the concentration of surface glycoproteins. T-cell receptor signaling, T-cell proliferation, TH1 differentiation, and CTLA-4 endocytosis are inhibited by Mgat5 branching. Non-T cells also contribute to MS pathogenesis and express abundant Mgat5 branched N-glycans. Here we explore whether Mgat5 deficiency in myelin-reactive T cells is sufficient to promote demyelinating disease. Adoptive transfer of myelin-reactive Mgat5−/− T cells into Mgat5+/+ versus Mgat5−/− recipients revealed more severe EAE in the latter, suggesting that Mgat5 branching deficiency in recipient naive T cells and/or non-T cells contribute to disease pathogenesis.

scholarly journals Rituximab Therapy Reduces Organ-Specific T Cell Responses and Ameliorates Experimental Autoimmune Encephalomyelitis

PLoS ONE ◽  
2011 ◽  
Vol 6 (2) ◽  
pp. e17103 ◽  
Author(s):  
Nancy L. Monson ◽  
Petra Cravens ◽  
Rehana Hussain ◽  
Christopher T. Harp ◽  
Matthew Cummings ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
T Cell Responses ◽  
Autoimmune Encephalomyelitis ◽  
Cell Responses ◽  
Organ Specific ◽  
Experimental Autoimmune
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