Autologous anti-CD19 CAR T-cell therapy (brexu-cel) that redirects patient T cells to kill CD19-positive B-lymphoblasts, inducing cytotoxicity and B-cell aplasia.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are retrovirally transduced to express an anti-CD19 scFv linked to CD28 costimulatory and CD3 zeta signaling domains. After infusion, CAR engagement of CD19 on B-lineage cells activates the T cells to proliferate and kill CD19-positive malignant B cells, leading to tumor lysis and on-target B-cell aplasia.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells and directly kill them via T-cell cytotoxicity (perforin/granzyme release and apoptosis via death receptor pathways).
Autologous dendritic cell vaccine generated ex vivo from a patient’s peripheral blood monocytes, differentiated into dendritic cells and pulsed with multiple EBV antigens to prime EBV-specific T-cell responses against EBV-positive nasopharyngeal carcinoma; dosed 5×10^6 cells subcutaneously every 2 weeks for 3–5 doses.
Autologous monocyte-derived dendritic cells pulsed ex vivo with EBV antigens are re-administered to present these antigens via MHC I/II, priming and expanding EBV-specific CD8+ cytotoxic T cells and CD4+ helper T cells. The resulting Th1/IFN-γ–biased response targets and lyses EBV-positive tumor cells in nasopharyngeal carcinoma.
YES
INDIRECT
DC vaccine primes EBV/LMP2A-specific CD8+ T cells that recognize LMP2A peptides on MHC I of EBV-positive tumor cells and kill them via perforin/granzyme (and Fas–FasL) cytotoxicity, driven by a Th1/IFN-γ response.
Autologous dendritic cell vaccine generated ex vivo from a patient’s peripheral blood monocytes, differentiated into dendritic cells and pulsed with multiple EBV antigens to prime EBV-specific T-cell responses against EBV-positive nasopharyngeal carcinoma; dosed 5×10^6 cells subcutaneously every 2 weeks for 3–5 doses.
Autologous monocyte-derived dendritic cells pulsed ex vivo with EBV antigens are re-administered to present these antigens via MHC I/II, priming and expanding EBV-specific CD8+ cytotoxic T cells and CD4+ helper T cells. The resulting Th1/IFN-γ–biased response targets and lyses EBV-positive tumor cells in nasopharyngeal carcinoma.
YES
INDIRECT
DC vaccine presents EBV antigens to prime EBV-specific CD8+ T cells; CTLs recognize LMP2B-derived peptides on MHC I of EBV+ cells and kill them via perforin/granzyme-mediated cytolysis (Th1/IFN-γ biased).
Autologous, fully human anti-CD19 CAR T-cell therapy engineered to eliminate CD19+ B-lineage cells to suppress B cell–driven autoimmunity in progressive MS.
Autologous anti-CD19 CAR T cells engineered with an scFv targeting CD19 and CD8alpha hinge/transmembrane, CD28 costimulatory, and CD3zeta signaling domains. After infusion, they bind CD19 on B-lineage cells, become activated, proliferate, and kill targets via cytotoxic mechanisms, selectively depleting CD19+ B cells to suppress B cell–driven autoimmunity.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells; CAR signaling activates T cells to kill via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
Autologous T cells engineered ex vivo to express a claudin 18.2-specific CAR; after infusion they bind CLDN18.2 on tumor cells and trigger MHC-independent T-cell activation, cytokine release, and cytotoxic killing in CLDN18.2-positive gastric/GEJ adenocarcinoma.
Autologous T cells are engineered ex vivo to express a CAR that binds claudin 18.2; upon encountering CLDN18.2 on tumor cells, the CAR triggers MHC-independent T-cell activation, cytokine release, and cytotoxic killing of CLDN18.2-positive cancer cells.
YES
DIRECT
CAR-T cells recognize CLDN18.2 and, upon activation, directly lyse target cells via perforin/granzyme release (and Fas–FasL apoptosis).