Autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are genetically engineered to express a CAR (with CD3ζ and costimulatory domains) that binds CD19; engagement triggers T-cell activation, proliferation, and perforin/granzyme-mediated cytotoxicity, eliminating CD19+ malignant B cells and causing expected B-cell aplasia. Administered by intravenous autotransfusion for relapsed/refractory CD19+ B-ALL/B-lymphoblastic lymphoma.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor containing CD3ζ and costimulatory domains. Upon binding CD19 on malignant B cells, the CAR triggers T-cell activation, expansion, and perforin/granzyme-mediated cytotoxicity, eliminating CD19+ cells and causing on‑target B‑cell aplasia.
CAR T cells bind CD19 and kill target cells via T-cell activation with perforin/granzyme-mediated cytolysis (and Fas/FasL), causing elimination of CD19+ cells.
Autologous CD19-directed CAR T-cell therapy. Patient T cells are modified to express a CAR with CD3ζ and costimulatory domains; upon binding CD19 on malignant B cells, they activate, expand, and kill targets via perforin/granzyme pathways, leading to depletion of CD19+ cells and B-cell aplasia. Given by intravenous autotransfusion for relapsed/refractory CD19+ B-ALL/B-lymphoblastic lymphoma.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor (CAR) containing CD3ζ and costimulatory domains. Upon binding CD19 on malignant B cells, CAR signaling activates and expands the T cells, which mediate cytotoxicity via perforin/granzyme, leading to targeted elimination of CD19+ cells and on‑target B‑cell aplasia.
CD19-directed CAR T cells bind CD19 on target cells, become activated, form an immune synapse, and kill via perforin/granzyme–mediated cytolysis (and Fas/FasL apoptosis).
Autologous CD19-directed CAR T-cell therapy. Engineered patient T cells express a CAR (CD3ζ with costimulatory domains) that recognizes CD19; receptor engagement triggers CAR/TCR signaling, T-cell proliferation, and targeted cytotoxicity, eradicating CD19+ malignant B cells and producing on-target B-cell aplasia. Administered via intravenous autotransfusion for relapsed/refractory CD19+ B-ALL/B-lymphoblastic lymphoma.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor (CD3ζ with costimulatory domains). Binding to CD19 activates the CAR, driving T-cell activation, expansion, and perforin/granzyme-mediated cytotoxicity to eliminate CD19-positive malignant B cells, with expected on-target B-cell aplasia.
CAR engagement of CD19 on target cells activates infused T cells, causing contact-dependent killing via perforin/granzyme (and Fas–FasL) pathways, lysing CD19+ cells.
Gene-modified natural killer cells engineered to express a chimeric antigen receptor targeting CD19 to deplete CD19+ B-lineage cells in refractory SLE.
Adoptive infusion of natural killer cells engineered with a chimeric antigen receptor specific for CD19 enables MHC-independent recognition of CD19 on B-lineage cells, triggering NK activation and cytotoxicity (perforin/granzyme and cytokines) to selectively deplete CD19+ B cells and plasmablasts, thereby reducing autoantibody production and B cell–driven inflammation in refractory SLE.
CAR-engineered NK cells recognize CD19 and kill target cells via NK degranulation (perforin/granzyme-mediated apoptosis).
Autologous tumor-infiltrating lymphocyte (TIL) therapy in which a patient’s tumor-resident T cells are expanded ex vivo and reinfused to mediate TCR-dependent cytotoxicity and cytokine release against tumor/HPV antigens, aiming to overcome tumor microenvironment immunosuppression.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are reinfused to recognize tumor/HPV antigens via native TCRs and mediate antitumor effects through cytotoxic killing (perforin/granzyme) and cytokine release (e.g., IFN-γ), aiming to overcome tumor microenvironment immunosuppression.
Patient-derived TILs recognize HPV E6 peptide presented on HLA via native TCR and directly kill target cells via perforin/granzyme-mediated cytolysis (and Fas/FasL, cytokine-mediated effects).