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

Grant‐Peters, Melissa; Passos, Giordani Rodrigues dos; Yeung, Hing‐Yuen; Jacob, Anu; Huda, Saif; Leite, Maria Isabel; Dendrou, Calliope A.; Palace, Jacqueline

doi:10.1002/acn3.51378

Cited by 16 publications

(7 citation statements)

References 21 publications

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“…This is in line with findings that CD4+ T cells (HLA class II) dominated cell infiltrates in MOGAD patients' lesions. In a Dutch and UK study, no negative association of MOGAD to an HLA subtype could be discerned to date, whereas a Chinese study suggested an association of DQB1 * 05:02-DRB1 * 16:02 alleles to pediatric-onset MOGAD ( 210 – 212 ). Notably, to this date, no definite genetic association could be shown in MOGAD; specifically, no strong HLA dependence, which is in contrast to what has been suggested in MS ( 210 – 212 ).…”

Section: Are Mog and Mog-igg-induced Animal Models Good Models For Mo...mentioning

confidence: 94%

Delimiting MOGAD as a disease entity using translational imaging

Oertel,

Hastermann,

Paul

2023

Front. Neurol.

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The first formal consensus diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) were recently proposed. Yet, the distinction of MOGAD-defining characteristics from characteristics of its important differential diagnoses such as multiple sclerosis (MS) and aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorder (NMOSD) is still obstructed. In preclinical research, MOG antibody-based animal models were used for decades to derive knowledge about MS. In clinical research, people with MOGAD have been combined into cohorts with other diagnoses. Thus, it remains unclear to which extent the generated knowledge is specifically applicable to MOGAD. Translational research can contribute to identifying MOGAD characteristic features by establishing imaging methods and outcome parameters on proven pathophysiological grounds. This article reviews suitable animal models for translational MOGAD research and the current state and prospect of translational imaging in MOGAD.

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Section: Are Mog and Mog-igg-induced Animal Models Good Models For Mo...mentioning

confidence: 94%

Delimiting MOGAD as a disease entity using translational imaging

Oertel,

Hastermann,

Paul

2023

Front. Neurol.

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“…In patients with MOGAD, genetic studies showed no strong correlation between human leukocyte antigen (HLA) genotype and MOGAD development; importantly, no cause for disease pathogenesis has been found. A recent study found a protective effect of the HLA-C*03:04 allele ( 44 ), whereas a Dutch study could not find any associations ( 45 ). In addition, in a Chinese cohort, there was an association between pediatric-onset MOGAD for DQB1*05:02-DRB1*16:02, but not for adult MOGAD ( 46 ).…”

Section: T- and B-cell Mediated Pathogenesis Of Myelin Oligodendrocyt...mentioning

confidence: 83%

The Potential Pathogenicity of Myelin Oligodendrocyte Glycoprotein Antibodies in the Optic Pathway

Lerch

Bauer²,

Reindl³

2022

Journal of Neuro-Ophthalmology

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Background: Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an acquired inflammatory demyelinating disease with optic neuritis (ON) as the most frequent clinical symptom. The hallmark of the disease is the presence of autoantibodies against MOG (MOG-IgG) in the serum of patients. Whereas the role of MOG in the experimental autoimmune encephalomyelitis animal model is well-established, the pathogenesis of the human disease and the role of human MOG-IgG is still not fully clear. Evidence Acquisition: PubMed was searched for the terms “MOGAD,” “optic neuritis,” “MOG antibodies,” and “experimental autoimmune encephalomyelitis” alone or in combination, to find articles of interest for this review. Only articles written in English language were included and reference lists were searched for further relevant papers. Results: B and T cells play a role in the pathogenesis of human MOGAD. The distribution of lesions and their development toward the optic pathway is influenced by the genetic background in animal models. Moreover, MOGAD-associated ON is frequently bilateral and often relapsing with generally favorable visual outcome. Activated T-cell subsets create an inflammatory environment and B cells are necessary to produce autoantibodies directed against the MOG protein. Here, pathologic mechanisms of MOG-IgG are discussed, and histopathologic findings are presented. Conclusions: MOGAD patients often present with ON and harbor antibodies against MOG. Furthermore, pathogenesis is most likely a synergy between encephalitogenic T and antibody producing B cells. However, to which extent MOG-IgG are pathogenic and the exact pathologic mechanism is still not well understood.

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“…A total of 26 patients with MOGAD were selected for this study with a slight female preponderance (male-to-female ratio of 1:1.36). The UK cohort ( 15 ) also showed a slight female preponderance of 62%, with an average age of onset of 31 years (range 3–69 years). In a multi-center study ( 16 ) involving at least three US race/ethnicities (white, black, Asian and other), the proportion of women was as high as 85% (21/25).…”

Section: Discussionmentioning

confidence: 97%

A retrospective study of myelin oligodendrocyte glycoprotein antibody-associated disease from a clinical laboratory perspective

Wang,

Danzeng,

Jiang

et al. 2023

Front. Neurol.

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ObjectivesTo analyze the differences in laboratory data between patients with myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD), multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD).MethodsThe study included 26 MOGAD patients who visited Beijing Tiantan Hospital from 2018 to 2021. MS and NMOSD patients who visited the clinic during the same period were selected as controls. Relevant indicators were compared between the MOGAD group and the MS/NMOSD groups, and the diagnostic performance of meaningful markers was assessed.ResultsThe MOGAD group showed a slight female preponderance of 57.7%, with an average onset age of 29.8 years. The absolute and relative counts of neutrophils were higher in the MOGAD group than in the MS group, while the proportion of lymphocytes was lower. The cerebrospinal fluid (CSF) IgG level, IgG index, 24-h IgG synthesis rate, and positive rate of oligoclonal bands (OCB) were lower in MOGAD patients than in the MS group. The area under ROC curve (AUC) was 0.939 when combining the relative lymphocyte count and IgG index. Compared to the NMOSD group, the MOGAD group had higher levels of serum complement C4 and lower levels of serum IgG. The AUC of serum C4 combined with FT4 was 0.783.ConclusionStatistically significant markers were observed in the laboratory data of MOGAD patients compared to MS/NMOSD patients. The relative lymphocyte count combined with IgG index had excellent diagnostic efficacy for MOGAD and MS, while serum C4 combined with FT4 had better diagnostic efficacy for MOGAD and NMOSD.

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

Cited by 16 publications

References 21 publications

Delimiting MOGAD as a disease entity using translational imaging

Delimiting MOGAD as a disease entity using translational imaging

The Potential Pathogenicity of Myelin Oligodendrocyte Glycoprotein Antibodies in the Optic Pathway

A retrospective study of myelin oligodendrocyte glycoprotein antibody-associated disease from a clinical laboratory perspective

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