Objectives: Multiple sclerosis (MS) is the most prevalent autoimmune disease of the central nervous system, and is characterized by inflammation and myelin damage. The immune system initiates the autoimmune response, although the mechanisms of neuronal damage have not been elucidated. The purpose of the present study was to investigate autoreactive CD4+ and CD8⁺ T lymphocytes, in conjunction with other inflammatory cells and cytokines in active MS lesions. Methods: EAE animal models was established by plantar injections of MBP (200 μg per rat). Purified CD4+ or CD8+ T-cells were isolated from heparinized peripheral blood (EAE animals and control animals) via negative selection. To examine effects of presence of autoreactive CD4+ and CD8+ T lymphocytes, we carried out ELISA, Western blot analysis and TUNEL. In addition, we examined the direct effects of various factors on neuronal cell death using MTT assay. Results: The data revealed that CD8+ T-cells were more toxic to neurons compared to CD4+ T-cells, in both the MBP and EAE conditions. Bax was greater increased when neurons were co-cultured with CD8+ T-cells in the MBP group. There is a significant increase in IL-17 secretion by CD4+ T-cells in both the MBP group and EAE group. Neuronal viability were affected by Perforin (1.5 μg/mL). Conclusion: The present study extends previous research by demonstrating the role of CD8+ T-cells in MS and supports perforin secretion by CD8+ T-cells as a potential therapeutic factor. Furthermore, we determined that CD4⁺ T-cells can enhance CD8⁺ T-cell neuronal cytotoxicity via induction of intense inflammation.

Background: Myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG) has been considered a diagnostic marker for patients with demyelinating disease, termed “MOG-IgG associated disorder” (MOGAD). Recently, the coexistence of MOG-IgG and other neuronal or glial antibodies has attracted extensive attention from clinicians. In this article, we systematically review the characteristics of MOG-IgG-related antibody coexistence syndrome. Methods: Two authors independently searched PubMed for relevant studies published before October 2021. We also manually searched the references of each related article. The appropriateness of the included studies was assessed by reading the titles, abstracts, and full texts if necessary. Results: Thirty-five relevant publications that met our inclusion criteria were finally included, of which fourteen were retrospective studies and twenty-one were case reports. A total of 113 patients were reported to show the coexistence of MOG-IgG and neuronal or glial antibodies. Additionally, 68.14% of patients were double positive for MOG-IgG and N-Methyl-D-Aspartate Receptor-IgG (NMDAR-IgG), followed by 23.01% of patients who were double positive for MOG-IgG and aquaporin4-IgG (AQP4-IgG). Encephalitis was the predominant phenotype when MOG-IgG coexisted with NMDAR-IgG, probably accompanied by imaging features of demyelination. Patients with dual positivity for MOG-IgG and AQP4-IgG experienced more severe disease and more frequent relapses. The coexistence of MOG-IgG and antibodies other than NMDAR-IgG and AQP4-IgG was extremely rare, and the clinical presentations were diverse and atypical. Except for patients who were double positive for MOG-IgG and AQP4-IgG, most patients with multiple antibodies had a good prognosis. Conclusions: MOG-IgG may coexist with neuronal or glial antibodies. Expanded screening for neuronal or glial antibodies should be performed in patients with atypical clinical and radiological features.

Background: Cognitive function impairment (CFI) and the Composite Dietary Antioxidant Index (CDAI) were investigated in this study.Methods: Participants from the 2011–2014 cycles of the National Health and Nutrition Examination Survey were chosen to assess cognitive function using the Consortium to Establish a Registry for Alzheimer’s Disease Word Learning Test, the Animal Fluency Test, and the Digit Symbol Substitution Test. Participants scored below the 25% percentile of any of the three tests were defined as having cognitive function impairment. 24-h recalls of diet were collected to calculate CDAI.Results: 2,424 participants were included. The fully adjusted multivariate logistic regression model showed an increase of one CDAI unit reduced CFI risk by 5% (95% CI: 0.92 ~ 0.98, p = 0.004). When comparing individuals with the lowest CDAI in the first quartile (<−2.42), the adjusted odds ratio for CDAI and CFI were 0.81 (95% CI: 0.61 ~ 1.06, p = 0.125) in the second quartile, 0.69 (95% CI: 0.51 ~ 0.92, p = 0.012) in the third quartile, and 0.59 (95% CI: 0.43 ~ 0.82, p = 0.002) in the fourth quartile, respectively. Restricted cubic spline analysis revealed a steady negative linear correlation between CDAI and CFI, with a p-value for non-linearity of 0.122. Subgroup analysis did not reveal any significant interactions based on age, education level, family income, history of diabetes, hypertension, stroke, and depression.Conclusion: CDAI was inversely associated with CFI in a large representative American population. Further longitudinal studies are needed for causal inference.