Targeted haploidentical neoantigen T-cell therapy: ex vivo–expanded donor-derived T cells (≥50% HLA match; HLA-A*02/11/24 alleles) primed to patient-specific tumor neoantigens to recognize and kill EBV-positive malignant T cells via TCR-mediated recognition and cytotoxic effector mechanisms.
Donor-derived haploidentical T cells are ex vivo expanded and primed/selected for reactivity to patient-specific tumor neoantigens. After infusion, they use native TCRs to recognize neoantigen peptides presented by HLA-A*02/11/24 on EBV-positive malignant T cells and eliminate them via perforin/granzyme-mediated cytotoxicity.
Adoptively transferred neoantigen-specific T cells recognize the patient-specific peptide presented by HLA-A*11 via their native TCR and kill the target cell through perforin/granzyme-mediated cytotoxicity.
Targeted haploidentical neoantigen T-cell therapy: ex vivo–expanded donor-derived T cells (≥50% HLA match; HLA-A*02/11/24 alleles) primed to patient-specific tumor neoantigens to recognize and kill EBV-positive malignant T cells via TCR-mediated recognition and cytotoxic effector mechanisms.
Donor-derived haploidentical T cells are ex vivo expanded and primed/selected for reactivity to patient-specific tumor neoantigens. After infusion, they use native TCRs to recognize neoantigen peptides presented by HLA-A*02/11/24 on EBV-positive malignant T cells and eliminate them via perforin/granzyme-mediated cytotoxicity.
Infused neoantigen-primed T cells recognize the patient-specific neoantigen peptide–HLA-A*24 complex via their native TCR and kill target cells through perforin/granzyme-mediated cytotoxicity.
Gene-modified cellular immunotherapy composed of CD19-directed chimeric antigen receptor (CAR) γδ T lymphocytes; given as a single IV dose (3×10^8–1×10^10 cells) to mediate cytotoxic lysis of CD19+ malignant B cells with anticipated on-target depletion of normal CD19+ B cells.
Allogeneic gamma-delta T lymphocytes are engineered via lentiviral transduction to express a CD19-directed chimeric antigen receptor. After IV infusion, CAR engagement of CD19 on B cells activates the gamma-delta T cells to mediate cytotoxic lysis of CD19-positive malignant B cells, with expected on-target depletion of normal CD19-positive B cells. Gamma-delta T cells function in an MHC-independent manner.
CD19 CAR-expressing gamma-delta T cells bind CD19 on B cells and kill them via T-cell effector mechanisms (perforin/granzyme and death-receptor pathways), leading to on-target lysis of CD19+ cells.
A bispecific IgG antibody immunotherapy that binds BCMA on malignant plasma cells and CD3 on T cells, forming an immune synapse to activate T cells and kill BCMA-positive tumor cells via cytotoxic granule release and cytokine-mediated responses.
Elranatamab is a bispecific IgG antibody that binds BCMA on malignant plasma cells and CD3 on T cells, bringing them into proximity to form an immune synapse. This activates T cells to kill BCMA-positive tumor cells via cytotoxic granule release and cytokine-mediated responses.
Elranatamab links CD3 on T cells to BCMA on target cells, forming an immune synapse and inducing T‑cell cytotoxicity via perforin/granzyme release and cytokine-mediated killing.
Allogeneic (off-the-shelf) bispecific CAR-modified natural killer (NK) cell therapy targeting BCMA and GPRC5D for multiple myeloma; single infusion after lymphodepletion to mediate cytotoxicity against malignant plasma cells.
Allogeneic bispecific CAR-engineered NK cells recognizing BCMA and GPRC5D on myeloma cells; CAR engagement activates NK cytotoxicity (perforin/granzyme, cytokines) to induce apoptosis of malignant plasma cells and mitigate antigen escape.
CAR-engineered NK cells recognize BCMA on target cells and induce NK cytotoxic killing via perforin/granzyme release and death-receptor pathways, leading to apoptosis.