Aimed to comprehensively investigate the presence of neural autoantibodies in the cerebrospinal fluid (CSF) and plasma of COVID-19 patients experiencing neurological complications during the Omicron wave in China. Forty consecutive COVID-19 patients with severe neurological complications and 15 disease controls (DC) were enrolled in the study. Neural autoantibodies were detected using both the indirect immunofluorescence assay (IFA) on mouse brain tissue and the Brain-neuronal-antigen microarray. A bioinformatics analysis was conducted to evaluate the similarity between SARS-CoV-2 proteins and the specific antigens identified by the microarray. Our results showed a markedly elevated prevalence of neural autoantibodies in CSF (62.16% vs. 0.0%) and in plasma of COVID-19 patients compared to DC using IFA. Additionally, we identified 12 upregulated intrathecal IgG autoantibodies with differential levels between COVID-19 patients and DC, as well as 51 upregulated IgG autoantibodies in plasma. Anti-mGluR2 antibodies exhibited the highest positivity rate in COVID-19 patients, a finding further confirmed by cell-based assays (CBA). Moreover, we discovered a shared peptide similarity between the SARS-CoV-2 N, S protein and mGluR2. Among two COVID-19 patients with positive anti-mGluR2 antibodies, there were specific and prominent bindings to both the RBD-Fc of S and mGluR2, while only weak binding was observed to N.

Background: C1q is a crucial component of the classical complement pathway. This study is the first to assess the association between disease activity and serum levels of C1q in Chinese Takayasu arteritis (TA) patients. Methods: Serum C1q levels in 190 TA patients and 154 healthy controls were assessed, and the relationship between serum C1q levels and indices of TA disease activity was analyzed. Moreover, we examined the correlation between serum C1q levels and two traditional inflammatory biomarkers; erythrocyte sedimentation rate (ESR) and hypersensitive CRP (hs-CRP). Results: Serum C1q levels were increased in TA patients compared with healthy controls (p=0.008). TA patients with active disease had higher levels of serum C1q than patients who had inactive disease (p<0.0001). Additionally, treatment-naïve patients had higher serum C1q levels than those who had been treated with corticosteroids or at least one immunosuppressant (p=0.001). Furthermore, a positive correlation between serum C1q levels and traditional inflammatory biomarkers in TA patients was found. The role of C1q in assessing disease activity was studied, and the area under the receiver operating characteristic (ROC) curve (AUC) of C1q for predicting active disease was 0.752,and a serum cutoff value of 167.15 mg/LC1q maximized the ability of disease activity assessment, with a sensitivity/specificity of 77.80%/64.90%. When the three indicators (C1q, ESR and hs-CRP) were combined, the AUC increased to 0.845, and the sensitivity to 84.40%. Conclusions: Serum C1q concentration may be a useful inflammatory marker for TA and a potential factor for evaluating disease activity in TA patients.