Neuromyelitis Optica Spectrum Disorders With Aquaporin-4 and Myelin-Oligodendrocyte Glycoprotein Antibodies

Kitley, J; Waters, Patrick; Woodhall, Mark; Leite, Maria Isabel; Murchison, Andrew G.; George, Jithin; Kuker, Wilhelm; Chandratre, S; Vincent, Angela; Palace, Jacqueline

doi:10.1001/jamaneurol.2013.5857

Cited by 535 publications

(569 citation statements)

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“…Evidence exists, however, for a subgroup of patients with NMO who are AQP4-IgG seronegative but myelin oligodendrocyte glycoprotein IgG seropositive, so AQP4-IgG seronegativity does not necessarily preclude a diagnosis of NMO. 64,65 Cerebrospinal fluid CSF exa mination will occasionally be necessary in patients presenting with symptoms of optic neuritis, principally when there is doubt as to the aetiology. CSF examination is rarely contributory in cases deemed to be MSON on other criteria.…”

Section: Immunological Pathologymentioning

confidence: 99%

The investigation of acute optic neuritis: a review and proposed protocol

et al. 2014

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| Optic neuritis is an inflammatory optic neuropathy that affects many patients with multiple sclerosis (MS) at some point during their disease course. Differentiation of acute episodes of MS-associated optic neuritis from other autoimmune and inflammatory optic neuropathies is vital for treatment choice and further patient management, but is not always straightforward. Over the past decade, a number of new imaging, laboratory and electrophysiological techniques have entered the clinical arena. To date, however, no consensus guidelines have been devised to specify how and when these techniques can be most rationally applied for the diagnostic work-up of patients with acute optic neuritis. In this article, we review the literature and attempt to formulate a consensus for the investigation of patients with acute optic neuritis, both in standard care and in research with relevance to clinical treatment trials.

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Section: Immunological Pathologymentioning

confidence: 99%

The investigation of acute optic neuritis: a review and proposed protocol

et al. 2014

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“…An association between commensal bacteria and host immunity is less well established in NMO patients, but a link is evident. For example, AQP4 is considered a primary autoimmune target in NMO (76), and AQP4-specific T cells show cross-reactivity to a protein product of C. perfringens (14).…”

Section: Gut Microbiota In Tnfr2mentioning

confidence: 99%

TNFR2 Deficiency Acts in Concert with Gut Microbiota To Precipitate Spontaneous Sex-Biased Central Nervous System Demyelinating Autoimmune Disease

Miller

Bonn

Franklin

et al. 2015

The Journal of Immunology

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TNF-α antagonists provide benefit to patients with inflammatory autoimmune disorders such as Crohn’s disease, rheumatoid arthritis, and ankylosing spondylitis. However, TNF antagonism unexplainably exacerbates CNS autoimmunity, including multiple sclerosis and neuromyelitis optica. The underlying mechanisms remain enigmatic. We demonstrate that TNFR2 deficiency results in female-biased spontaneous autoimmune CNS demyelination in myelin oligodendrocyte glycoprotein–specific 2D2 TCR transgenic mice. Disease in TNFR2−/− 2D2 mice was associated with CNS infiltration of T and B cells as well as increased production of myelin oligodendrocyte glycoprotein–specific IL-17, IFN-γ, and IgG2b. Attenuated disease in TNF−/− 2D2 mice relative to TNFR2−/− 2D2 mice identified distinctive roles for TNFR1 and TNFR2. Oral antibiotic treatment eliminated spontaneous autoimmunity in TNFR2−/− 2D2 mice to suggest role for gut microbiota. Illumina sequencing of fecal 16S rRNA identified a distinct microbiota profile in male TNFR2−/− 2D2 that was associated with disease protection. Akkermansia muciniphila, Sutterella sp., Oscillospira sp., Bacteroides acidifaciens, and Anaeroplasma sp. were selectively more abundant in male TNFR2−/− 2D2 mice. In contrast, Bacteroides sp., Bacteroides uniformis, and Parabacteroides sp. were more abundant in affected female TNFR2−/− 2D2 mice, suggesting a role in disease causation. Overall, TNFR2 blockade appears to disrupt commensal bacteria–host immune symbiosis to reveal autoimmune demyelination in genetically susceptible mice. Under this paradigm, microbes likely contribute to an individual’s response to anti-TNF therapy. This model provides a foundation for host immune–microbiota-directed measures for the prevention and treatment of CNS-demyelinating autoimmune disorders.

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“…This suggests that cord involvement may occur without clinical or radiologic evidence of myelitis. The use of full-length human MOG in our cellbased assay as opposed to C-terminal truncated human MOG used by other groups 23,38 may account for some differences in findings. In addition, 14/23 AQP4 antibody-negative patients with NMO/NMOSD in our cohort were also MOG antibody-negative, suggesting there may be other antigen targets.…”

mentioning

confidence: 95%

“…[14][15][16][17][18] In contrast, the clinical relevance of MOG antibodies in adults is unclear, as only a minority of patients with MS and NMO/NMOSD are seropositive. 16,[18][19][20][21][22][23][24] Herein, we provide evidence that MOG antibodies are a clinical biomarker of bilateral and/ or recurrent optic neuritis (BON) in adults and describe the characteristic clinical course, response to therapy, and visual outcomes of this condition.…”

mentioning

confidence: 99%

“…In our cohort, the 9 MOG antibody-positive patients did not have intrathecal oligoclonal bands or radiology consistent with MS, suggesting that this condition may be an immunologic entity that is distinct from both AQP4 antibody-positive NMO and MS. While we did not test a cohort of AQP4 antibodypositive patients for MOG antibodies in the context of this study, AQP4-and MOG-antibody double positivity has been seldom reported 23,24,39,40 ; therefore, the evaluation of the prevalence and clinical significance of double seropositive patients is a point of interest for future work.…”

mentioning

confidence: 99%

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