Abstract
Objective: T lymphocytes, complement, and immunoglobulin play an important role in neuromyelitis optica spectrum disorders (NMOSD). As common clinical examination indicators, they have been used as routine indicators in many hospitals, which is convenient for being carried out in clinical work, but there are few articles of guiding significance for clinical practice. The purpose of this study was to study the relationship between commonly used immune indicators and clinical characteristics in patients with NMOSD. Methods: We compared clinical characteristics and clinical immune indicators in 258 patients with NMOSD and 200 healthy controls (HCs). We used multiple linear regression to study the relationship between immunotherapy, disease phase, sex, age, AQP4-IgG, and immune indicators. In addition, lymphocyte subsets were compared before and after immunotherapy in 24 of the 258 patients. We explored the influencing factors and predictors of severe motor disability. Results: The percentages of CD3 ratio (71.4% vs. 73.8%, p = 0.013), CD4 ratio (38.8% vs. 42.2%, p < 0.001), and CD4/CD8 ratio (1.43 vs. 1.66, p < 0.001) in NMOSD patients were significantly lower than those in the HC group. In addition, complement C4 (0.177 g/L vs. 0.221 g/L, p < 0.001) and peripheral blood IgG (10.95 g/L vs. 11.80 g/L, p = 0.026) in NMOSD patients were significantly lower than those in the HC group. CD3 percentage was correlated with blood collection age and disease stage; CD8 percentage was correlated with blood collection age, disease stage, and treatment; CD4/CD8 percentage was correlated with blood collection age and treatment; complement C4 was correlated with blood collection age and sex; and IgG was correlated with disease stage and treatment. Twenty-four patients before and after treatment showed that the percentages of CD3 ratio (74.8% vs. 66.7%, p = 0.001) and CD8 ratio (32.4% vs. 26.2%, p < 0.001) after treatment in NMOSD patients were significantly increased, and the percentage of CD3 before treatment was moderately negatively correlated with ARR (r = −0.507, p = 0.011). Binary logistic regression analysis showed that peripheral blood complement C3 is a serious influencing factor for severe motor disability (EDSS score ≥ 6 points). Peripheral blood complement C3 and C4 are predictors of severe motor disability (p < 0.05). Conclusion: Our results suggest that peripheral blood T lymphocytes, C3, C4 and immunoglobulin are convenient and routine clinical indicators that are convenient for implementation in clinical work. They have certain reference values for disease staging, recurrence, drug efficacy, and motor disability. They have improved our understanding of clinical immune indicators for NMOSD patients, but whether they can be used as biomarkers for clinical prognosis remains to be further studied.
Highlights
Neuromyelitis optica spectrum disorders (NMOSD) is considered an autoimmune and inflammatory disease of the central nervous system (CNS) that primarily attacks the optic nerve and spinal cord [1,2]
T lymphocytes, complement, and immunoglobulin play an important role in the occurrence and development of NMOSD
We found correlation between between T lymphocyte subsets and disease activity in patients with NMOSD in this study, between and disease activity in patients with in this study, and disease activity in patients with in this study, and and we found that immunotherapy was associated with an increase in T lymphocyte suband we found that immunotherapy was associated with an increase in
Summary
Neuromyelitis optica spectrum disorders (NMOSD) is considered an autoimmune and inflammatory disease of the central nervous system (CNS) that primarily attacks the optic nerve and spinal cord [1,2]. Most studies believed that NMOSD is a central nervous system inflammation mainly mediated by B cells, but the role of T cells in NMOSD has received attention in recent years. Disruption of the blood–brain barrier (BBB) is the first critical step in the pathogenesis of NMOSD, allowing the influx of humoral factors, including autoantibodies, through the dysfunctional barrier and infiltration of inflammatory cells [6]. In these ways, T lymphocytes, complement, and immunoglobulin play an important role in the occurrence and development of NMOSD
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