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J Biomol Struct Dyn ; 39(7): 2526-2542, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32242486

RESUMO

The main pathologic hallmark of multiple sclerosis is a demyelinating plaque that contains a prominent immunologic response dominated by T cells of the immune system. PLP (proteolipid protein), MPB (myelin basic protein), and Myelin oligodendrocyte glycoprotein (MOG) proteins are important autoantigens for the demyelinating of CNS in multiple sclerosis. There is good evidence indicating that T CD8+ cells and MHC class I molecules play an important role in this disease. The HLA-A*31:01 allele of MHC class I is a member of HLA-A3 superfamily and there is no clear report concerning the relationship of this allele with MS. Feeling this gap, we studied the possible association of the HLA-A*31:01 with MS by prediction of neuroantigenic epitopes of human MBP, PLP, and MOG proteins of myelin sheath using in silico methods. PLP did not show any neuroantigenic epitope, but the two epitopes of MBP and seven epitopes of MOG for HLA-A*31:01 were determined via bioinformatics servers. In silico study of the nine epitope showed that MOG195-204 (LIICYNWLHR) peptide of the membrane-associated/cytoplasmic part of human MOG has suitable binding affinity to the HLA-A*31:01 allele as a potential neuroantigenic epitope. Further investigations of this peptide revealed that the binding of C-terminal residue of this peptide has a more significant effect on binding to this allele than the N-terminal part of the peptide. Altogether, this combination of "LIICYNWLHR/A*31:01 allele "may play an important role in MS pathogenesis and this complex is suggested for further studies such as T cell receptor.Communicated by Ramaswamy H. Sarma.


Assuntos
Antígenos HLA-A/genética , Esclerose Múltipla , Alelos , Simulação por Computador , Proteínas de Ligação a DNA/genética , Epitopos de Linfócito T/genética , Humanos , Esclerose Múltipla/genética , Proteína Básica da Mielina/genética , Glicoproteína Associada a Mielina/genética , Glicoproteína Mielina-Oligodendrócito/genética , Fatores de Transcrição/genética
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