No strong HLA association with MOG antibody disease in the UK population

Improvements in assays for detecting serum antibodies against myelin oligodendrocyte glycoprotein (MOG) have led to the appreciation of MOG‐antibody‐associated disease (MOGAD) as a novel disorder. However, much remains unknown about its etiology. We performed human leukocyte antigen (HLA) analysis i...

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Detalles Bibliográficos
Autores principales: Grant‐Peters, Melissa, Passos, Giordani Rodrigues Dos, Yeung, Hing‐Yuen, Jacob, Anu, Huda, Saif, Leite, Maria Isabel, Dendrou, Calliope A., Palace, Jacqueline
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Brief Communications
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8283171/
https://www.ncbi.nlm.nih.gov/pubmed/33991459
http://dx.doi.org/10.1002/acn3.51378
Descripción
Sumario:Improvements in assays for detecting serum antibodies against myelin oligodendrocyte glycoprotein (MOG) have led to the appreciation of MOG‐antibody‐associated disease (MOGAD) as a novel disorder. However, much remains unknown about its etiology. We performed human leukocyte antigen (HLA) analysis in 82 MOGAD patients of European ancestry in the UK population. No HLA class II associations were observed, thus questioning the mechanism of anti‐MOG antibody generation. A weak protective association of HLA‐C*03:04 was observed (OR = 0.26, 95% CI = 0.10‐0.71, p(c)  = 0.013), suggesting a need for continued efforts to better understand MOGAD genetics and pathophysiology.

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