Pediatric systemic lupus erythematosus (SLE) is associated with high disease severity and significantly higher morbidity and mortality compared to adult-onset SLE, making it a particularly challenging condition to manage. Chimeric antigen receptor (CAR) T-cell therapy holds significant promise for improving outcomes in refractory pediatric SLE. However, the use of CAR T-cell therapy in pediatric patients presents unique challenges, including difficulty in collecting sufficient T cells. Pediatric patients may experience distinct side effects, such as age-specific toxicities or more pronounced neurotoxic events, requiring tailored monitoring and management. Additionally, the psychological impact on children and their families, facing potentially life-threatening treatment protocols, must be carefully addressed. To date, only four children with SLE have been treated with CAR T cells, highlighting the early stage of research in this area. The clinical outcomes provide hope that CAR T-cell therapy could offer a breakthrough in treating pediatric SLE; however, main limitations remain the small number of patients and the relatively short follow-up. More data are needed to fully assess the safety, efficacy, and long-term outcomes in this vulnerable population. Key Points• Pediatric SLE is characterized by more severe manifestations, higher morbidity, and increased mortality compared to adult-onset SLE. • CAR T-cell therapy shows promise as a potential treatment for refractory pediatric SLE aiming ideally towards long-term, drug-free remission. • CAR T-cell therapy in pediatric SLE presents unique challenges, including age-related toxicities, technical difficulties, and ethical considerations. • To date, results are available from only a handful of children with SLE treated with CAR T cells. Expected advancements in CAR T-cell technology, along with data from ongoing clinical trials involving children with SLE, will determine the pace and extent of CAR T-cell therapy application in pediatric SLE.
30 March 2026 in Journal of Mosaic of Autoimmunity
Environmental triggers, particularly viral infections such as Epstein-Barr virus (EBV), may significantly contribute to the induction or exacerbation of psoriasis (Ps). EBV persists lifelong and is linked to several autoimmune diseases. Nuclear antigen 1 (EBNA-1) helps maintain latency and is a key immune target. Objective: This study aimed to investigate the potential association between EBV infection, specifically the humoral immune response to EBNA-1, and psoriasis by comparing seroprevalence and antibody levels in psoriatic patients versus healthy controls. Methods: A case-control study was conducted involving 23 patients with psoriasis (Ps) and 22 healthy controls (HC). Serum samples were analyzed for the presence of anti-EBNA-1 IgG antibodies using a standard enzyme-linked immunosorbent assay (ELISA). Seropositivity rates were compared using Fisher’s Exact Test, and quantitative antibody levels, expressed as mean ± standard deviation, were compared using an appropriate parametric test. Results: A significantly higher proportion of psoriatic patients were seropositive for anti-EBNA-1 antibodies than healthy controls (95.7% vs. 59.1%, p = 0.004). However, among seropositive individuals, the mean quantitative antibody levels did not differ significantly between the two groups (Ps: 63 ± 25.7 vs. HC: 75.6 ± 31.6, p = ns). Conclusion: Anti-EBNA-1 EBV antibodies are more prevalent in psoriasis compared to healthy controls, and further research is warranted to elucidate the mechanistic role of that viral antigen as a potential contributor to disease-related immune inflammation.