Autologous, gene-modified Tmod logic-gated CAR T-cell therapy with an MSLN-targeting activating receptor and an HLA-A*02–specific inhibitory receptor, designed to selectively kill mesothelin-positive tumor cells with loss of HLA-A*02 while sparing normal tissues.
Autologous, gene‑modified logic‑gated CAR T cells with an MSLN‑targeting activating CAR and an HLA‑A*02–specific inhibitory receptor (Tmod) that enable killing of mesothelin‑positive tumor cells that have lost HLA‑A*02 while sparing HLA‑A*02–positive normal tissues; includes B2M shRNA to modulate HLA class I on the engineered T cells. Anti‑tumor effect via redirected T‑cell cytotoxicity (perforin/granzyme, cytokines).
MSLN-positive tumor cells lacking HLA-A*02 are recognized by the activating anti-mesothelin CAR and are lysed by the engineered T cells via perforin/granzyme-mediated cytotoxicity (with cytokine effects). The HLA-A*02–specific inhibitory receptor blocks killing of HLA-A*02–positive cells.
Autologous anti-CD19 CAR T-cell therapy (Tecartus) that targets CD19-positive B-ALL blasts and eliminates them via CAR-mediated activation and cytotoxic effector mechanisms.
Autologous T cells are retrovirally engineered to express an anti-CD19 chimeric antigen receptor with a CD28 costimulatory domain and CD3 zeta signaling domain; upon binding CD19 on malignant B cells, the CAR T cells activate, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity to eliminate CD19-positive leukemia cells.
Anti-CD19 CAR T cells bind CD19 on target cells, activate, and kill them via perforin/granzyme-mediated cytolysis (apoptosis).
Autologous anti-CD19 chimeric antigen receptor T-cell therapy that recognizes CD19 on malignant B cells, activates T cells, and mediates cytotoxic killing.
Autologous anti-CD19 chimeric antigen receptor T cells that recognize CD19 on malignant B cells, activate and expand upon engagement, and mediate cytotoxic killing of CD19-positive cells via perforin/granzyme pathways and cytokine-driven immune responses.
Anti-CD19 CAR T cells bind CD19 on target cells, activate, and induce cytotoxic killing via perforin/granzyme-mediated apoptosis (and Fas/FasL and cytokine effector pathways).
Autologous adoptive T-cell therapy consisting of ex vivo expanded CD8+/CD4+ T cells specific for patient tumor neoantigen peptides; TCR recognition of neoantigen–HLA on tumor cells triggers cytotoxic killing and IFN-γ–mediated effects to boost tumor-specific immunity.
Autologous CD8+/CD4+ T cells are isolated and expanded ex vivo for specificity to patient tumor neoantigen peptides. After infusion, native TCRs recognize neoantigen–HLA complexes on tumor cells, triggering perforin/granzyme-mediated cytotoxicity and IFN-γ–driven immune activation to enhance tumor-specific immunity.
Infused neoantigen‑reactive T cells recognize the neoantigen–HLA class I complex via their native TCRs and kill target cells through perforin/granzyme-mediated cytotoxicity (and related CTL apoptotic pathways).
Autologous adoptive T-cell therapy consisting of ex vivo expanded CD8+/CD4+ T cells specific for patient tumor neoantigen peptides; TCR recognition of neoantigen–HLA on tumor cells triggers cytotoxic killing and IFN-γ–mediated effects to boost tumor-specific immunity.
Autologous CD8+/CD4+ T cells are isolated and expanded ex vivo for specificity to patient tumor neoantigen peptides. After infusion, native TCRs recognize neoantigen–HLA complexes on tumor cells, triggering perforin/granzyme-mediated cytotoxicity and IFN-γ–driven immune activation to enhance tumor-specific immunity.
Native TCRs on infused neoantigen‑reactive T cells recognize the neoantigen–HLA class II complex and directly lyse target cells via perforin/granzyme (± Fas–FasL) pathways, with supportive IFN-γ effects.