eligibility_summary
Eligible: 3–65 yrs with SLE per 2019 EULAR/ACR, ANA ≥1:80 and/or anti‑dsDNA ≥30 IU/mL, refractory SLE (SLEDAI‑2K ≥8 or steroid‑dependent and failed standard therapy) and/or biopsy‑proven class III/IV (non‑C) or V+III/IV LN, CD19+ B cells, lymphocytes >1×10^9/L, off immunosuppression ≥7 d, ECOG 0–2, life ≥90 d, consent. Exclude: major CNS/cardiac/respiratory disease, active infection (hepatitis/HIV/syphilis), malignancy, DIC, uncontrolled DM, severe psych illness, pregnancy/lactation, eGFR <30, confounding skin disease, prior organ transplant (except SCT), no PBMC.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: autologous anti‑CD19 chimeric antigen receptor T cells (CD19 CAR‑T) given once after lymphodepleting cyclophosphamide + fludarabine. Drug type: genetically engineered cell therapy (adoptive T‑cell immunotherapy). Mechanism: patient T cells are modified to express a CAR that binds CD19, triggering targeted cytotoxicity and expansion upon antigen engagement to deplete CD19+ B‑lineage cells, aiming to eliminate autoreactive B cells/plasmablasts and reset humoral immunity in refractory SLE/lupus nephritis. Targets: CD19-expressing B cells (naive, memory, germinal center B cells, plasmablasts/early plasma cells). Pathways impacted: BCR-driven autoantibody production (ANA, anti‑dsDNA), immune complex/complement activation, and B–T cell costimulation, lymphodepletion enhances CAR‑T engraftment via homeostatic cytokines. Single‑arm phase 1/2, primary endpoints: DLTs (phase 1) and overall response rate (phase 2).