scholarly journals WITHDRAWN: IFN-γ and IL-1β treated-human placenta-derived mesenchymal stromal cells enhance the generation of IL-10+T cells by upregulating PDLs expressions and ameliorate experimental autoimmune encephalomyelitis

Oncotarget ◽  
2018 ◽  
Vol 0 (0) ◽  
Author(s):  
Zhuoya Wang ◽  
Zhuoya Wang ◽  
Weiwei Wang ◽  
Weiwei Wang ◽  
Yun Hou ◽  
...  







PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e65913 ◽  
Author(s):  
Rodolfo Thomé ◽  
Adriel S. Moraes ◽  
André Luis Bombeiro ◽  
Alessandro dos Santos Farias ◽  
Carolina Francelin ◽  
...  


2013 ◽  
Vol 191 (1) ◽  
pp. 117-126 ◽  
Author(s):  
Sterling B. Ortega ◽  
Venkatesh P. Kashi ◽  
Andrew F. Tyler ◽  
Khrishen Cunnusamy ◽  
Jason P. Mendoza ◽  
...  


2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Ani Grigorian ◽  
Michael Demetriou

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.



2011 ◽  
Vol 187 (3) ◽  
pp. 1120-1128 ◽  
Author(s):  
Young H. Kim ◽  
Beom K. Choi ◽  
Su M. Shin ◽  
Chang H. Kim ◽  
Ho S. Oh ◽  
...  




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