A protective effect of lower MHC-II expression in MOGAD.

Myelin oligodendrocyte glycoprotein-antibody-associated disease (MOGAD) is a demyelinating central nervous system disorder. We aimed to uncover immune pathways altered in MOGAD to predict disease progression. Using nanostring nCounter technology, we analyzed immune gene expression in PBMCs from MOGAD patients and compare it with healthy controls (HCs). We found 35 genes that distinguished MOGAD patients and HCs. We then validated those results in a larger cohort including MS and NMOSD patients. Expressions of HLA-DRA was significantly lower in MOGAD patients. This reduction in HLA-DRA, correlated with a monophasic disease course and greater brain volume, enhancing our ability to predict MOGAD progression.

Altered immune co-inhibitory receptor expression and correlation of LAG-3 expression to disease severity in NMOSD.

Co-inhibitory receptors (CIR)s regulate T cell-mediated immune responses and growing evidence links co-inhibitory receptors to the progression of neuroimmunological diseases. We studied the expression levels of CIRs: TIM-3, TIGIT, PD-1 and LAG-3 in the peripheral blood mononuclear cells (PBMCs) of 30 patients with Neuromyelitis optica spectrum disorder (NMOSD), 11 Multiple sclerosis (MS) patients and 31 Healthy controls (HC). We found that the mRNA expression levels of TIM-3 were significantly increased in NMOSD compared with HC, and increased LAG-3 surface protein expression was also observed on T-cells of NMOSD patients. Moreover, we observed a negative correlation between LAG-3 expression and disease severity in NMOSD. Our findings suggest a protective effect of LAG-3 in the setting of NMOSD, and that the differential expression of CIRs observed in this study may play a role in the pathological process of NMOSD.

Thyroid hormone dysfunction in MOGAD and other demyelinating diseases.

BACKGROUND: Thyroid hormones play a critical role in both neuronal and glial cell functions. Multiple sclerosis (MS) has increased co-occurrence with autoimmune thyroid diseases, and recent studies have suggested a potential link between neuromyelitis optica spectrum disorder (NMOSD) and thyroid hormones. However, no previous studies have examined the relationship between thyroid hormones and myelin oligodendrocyte glycoprotein-associated demyelination (MOGAD). METHODS: We investigated the role of thyroid hormones in central nervous system (CNS) autoimmune demyelinating diseases in 26 MOGAD patients, 52 NMOSD patients, 167 patients with MS, and 16 patients with other noninflammatory neurological disorders. Thyroid hormone levels and clinical data (Expanded Disability Status Scale [EDSS]) were analyzed. Volumetric brain information was determined in brain magnetic resonance imaging (MRI) using the MDbrain platform. RESULTS: MOGAD patients had significantly higher levels of free triiodothyronine (FT3) compared to NMOSD patients. No correlation was found between FT3 levels and disease severity or brain volume. Thyroid-stimulating hormone (TSH) levels did not differ significantly between the groups, but in NMOSD patients, higher TSH levels were associated with lower disability scores and increased brain volume. No significant differences in free thyroxine (FT4) levels were observed between the different groups, however, FT4 levels were significantly higher in relapsing versus monophasic MOGAD patients and increased FT4 levels were associated with a higher EDSS and lower brain volume in NMOSD patients. CONCLUSION: Our findings highlight the potential involvement of thyroid hormones specifically in MOGAD patients and other demyelinating CNS disorders. Understanding the role of thyroid hormones in relapsing vs monophasic MOGAD patients and in comparison to other demyelinating disorder could lead to the development of therapeutic interventions. Further studies are needed to explore the precise mechanisms and potential interventions targeting the thyroid axis as a treatment strategy.

COVID-19 in Cladribine-treated patient with multiple sclerosis.

Case report describing a patient infected with COVID-19 after initiation of Cladribine, with a favorable disease course and positive seroconversion.

MIF -173G/C polymorphism is associated with NMO disease severity.

Our knowledge about genetic factors that drive the worsening of neuromyelitis optica (NMO) is limited. Herein, we analyzed the macrophage migration inhibitory factor (MIF) -173G/C functional polymorphism in NMO patients and controls. Our data reveal that the frequency of the high-expression MIF genotypes (CC/GC) did not differ between the two groups. However, frequency of this genotypes was elevated in patients diagnosed with both optic neuritis and myelitis compared with patients that were diagnosed with only one symptom. Furthermore, patients carrying the CC/CG genotypes had significantly higher disability score. We conclude that MIF is associated with NMO severity rather than susceptibility.