Aberrant Immune Features after Recovery from COVID-19 in Patients with Systemic Lupus Erythematosus and Other Autoimmune Diseases

• Published in: Biomedicines 2023-10, Vol.11 (10), p.2807
• Main Authors: Yu, Siyue, Li, Hao, Zhang, Kai, Cheng, Gong, Wang, Yifan, Jia, Yuan, Su, Linchong, Jin, Yuebo, Shao, Miao, He, Jing
• Format: Article
• Language: English
• Subjects: Autoimmune diseases; B cells; broad immune response; Care and treatment; CD4 antigen; Coronaviruses; COVID-19; COVID-19 vaccines; Development and progression; Disease; Flow cytometry; Foxp3 protein; Guillain-Barre syndrome; Health aspects; Helper cells; Hospitals; Immune status; Immune system; Immunology; immunology mechanisms; Immunoregulation; Infections; Leukocytes (mononuclear); Long-term effects; Lupus; Lymphocytes; Lymphocytes T; Medical laboratories; Medical research; Medicine, Experimental; pandemic influenza; Patients; Proteins; regulatory T cell; Rheumatoid arthritis; Severe acute respiratory syndrome coronavirus 2; Systemic lupus erythematosus; T cells
• ISSN: 2227-9059; 2227-9059
• DOI: 10.3390/biomedicines11102807

Considering the large number of individuals who have already been infected and may have reinfection, the post-infection effects of COVID-19 are of great importance for clinical practice and predicting disease trends. However, our understanding of the potential long-term effects, particularly on immunity, after recovering from COVID-19 remains limited. The aim of this study was to investigate the abnormal immunological factors that contribute to the prolonged immunological effects of COVID-19. Two groups of patients were enrolled in the study, including 11 individuals with various autoimmune diseases (AIDs) and 16 patients diagnosed with systemic lupus erythematosus (SLE). Detailed clinical symptoms were closely monitored, and peripheral mononuclear cells were analyzed using flow cytometry. The clinical status was evaluated using the SLE Disease Activity Index (SLEDAI) and the Clinical Global Impressions (CGI) index. The proportions of follicular T helper cells (Tfh) exhibited significant increases in both cohorts (AID: p = 0.03; SLE: p = 0.0008). Conversely, the percentages of Foxp3+ and CD4+ regulatory T cells (Treg) were reduced in patients following COVID-19 infection (AID: p = 0.009, 0.05, resp.; SLE: p = 0.02, 0.0009, resp.). The percentages of Th2 and Th17 cells were significantly increased in SLE patients (p < 0.05). Exacerbated conditions were observed in SLE patients two months after infection (SLEDAI, p < 0.05). Our findings show that COVID-19 infection increases Tfh cells and decreases Treg cells in patients of AIDs, worsening pathogenetic immune status in post-recovery populations.