Investigational autologous anti-CD22 CAR T-cell therapy infused 28–42 days after tisagenlecleucel; engineered T cells target CD22 to eliminate residual or antigen-shifted B-ALL via CAR-mediated T-cell activation and cytotoxicity.
Autologous T cells engineered to express a chimeric antigen receptor targeting CD22 on B-lineage cells. Upon CD22 binding, the CAR (CD3z with costimulation) activates the T cell, driving expansion, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate CD22-positive malignant B cells, including residual or antigen-shifted blasts after CD19-directed therapy.
YES
DIRECT
Anti-CD22 CAR T cells bind CD22, become activated via CAR signaling, and kill target cells through perforin/granzyme-mediated cytolysis and death-receptor (e.g., Fas/FasL) apoptosis.
Injectable bispecific T‑cell–engaging antibody that binds GPRC5D on myeloma plasma cells and CD3 on T cells to activate TCR/CD3 signaling and redirect cytotoxic T cells to kill GPRC5D-positive malignant plasma cells.
Bispecific T-cell–engaging antibody that binds GPRC5D on myeloma cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and redirect cytotoxic T cells to kill GPRC5D-positive malignant plasma cells via perforin/granzyme release.
YES
DIRECT
Bispecific T‑cell engager binds GPRC5D on target cells and CD3 on T cells, forming an immune synapse that activates T cells to release perforin and granzymes, killing GPRC5D-positive cells.
Injectable bispecific T‑cell–engaging antibody that binds GPRC5D on myeloma plasma cells and CD3 on T cells to activate TCR/CD3 signaling and redirect cytotoxic T cells to kill GPRC5D-positive malignant plasma cells.
Bispecific T-cell–engaging antibody that binds GPRC5D on myeloma cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and redirect cytotoxic T cells to kill GPRC5D-positive malignant plasma cells via perforin/granzyme release.
NO
INDIRECT
Binds CD3 on T cells to activate and bridge them to GPRC5D+ myeloma cells, which are then killed via perforin/granzyme release; CD3+ T cells are not targeted.
Autologous BCMA-directed CAR T-cell therapy; patient T cells are engineered with a 4-1BB/CD3ζ chimeric antigen receptor targeting BCMA (TNFRSF17) to activate T cells and mediate cytotoxic killing of myeloma cells.
Autologous T cells engineered to express a BCMA-targeted CAR with 4-1BB costimulatory and CD3ζ signaling domains; upon binding BCMA on malignant plasma cells, the CAR T cells activate, proliferate, and mediate cytotoxic killing of myeloma cells.
YES
DIRECT
BCMA-directed CAR T cells bind BCMA on target cells, activate via CD3ζ/4-1BB signaling, and kill through perforin/granzyme-mediated cytolysis and apoptosis pathways.
Autologous dendritic cell tumor vaccine in which patient-derived dendritic cells are loaded with tumor antigens to enhance antigen presentation and activate CD8+ and CD4+ T cells to kill glioma/GBM cells.
Autologous dendritic cells are loaded with patient tumor antigens and reinfused to enhance MHC I/II antigen presentation and co-stimulation, activating tumor-specific CD8+ cytotoxic and CD4+ helper T cells to drive immune-mediated killing of glioma/GBM cells.
YES
INDIRECT
DC vaccine primes tumor-specific CD8+ T cells that recognize neoantigen peptides presented on HLA-I and kill target cells via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.