Autologous dendritic-cell cancer vaccine transduced with an adenoviral vector encoding HER2 ECD/TMD to present HER2 and prime HER2-specific T cells and antibodies.
Autologous dendritic cells are transduced ex vivo with an adenoviral vector encoding the HER2 extracellular and transmembrane domains, enabling the DCs to express, process, and present HER2 antigens on MHC I and II with costimulation. After administration, these DCs prime and expand HER2-specific CD8+ cytotoxic T cells and CD4+ helper T cells and can induce anti-HER2 antibodies, generating tumor-specific immunity against HER2-positive cancers.
YES
INDIRECT
Vaccine-primed HER2-specific CD8+ T cells recognize HER2 peptides on MHC I and kill HER2+ cells via perforin/granzyme; induced anti-HER2 antibodies can mediate ADCC/complement.
Anti‑CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Autologous, lentiviral-engineered chimeric antigen receptor T-cell therapy with a bicephalic APRIL/BAFF ligand domain enabling dual recognition of BCMA and TACI (and possibly BAFF-R) on malignant plasma cells to trigger T-cell activation and cytotoxicity.
Autologous T cells are lentivirally engineered to express a chimeric antigen receptor with a bicephalic APRIL/BAFF ligand domain that binds BCMA and TACI (and possibly BAFF-R) on malignant plasma cells. Receptor engagement activates CAR signaling (CD3ζ with costimulation), leading to T‑cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape compared with single-antigen CARs.
YES
DIRECT
CAR-T cells bind BCMA via the APRIL/BAFF ligand domain, triggering CAR signaling and T‑cell effector functions that kill BCMA+ cells by perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Autologous, lentiviral-engineered chimeric antigen receptor T-cell therapy with a bicephalic APRIL/BAFF ligand domain enabling dual recognition of BCMA and TACI (and possibly BAFF-R) on malignant plasma cells to trigger T-cell activation and cytotoxicity.
Autologous T cells are lentivirally engineered to express a chimeric antigen receptor with a bicephalic APRIL/BAFF ligand domain that binds BCMA and TACI (and possibly BAFF-R) on malignant plasma cells. Receptor engagement activates CAR signaling (CD3ζ with costimulation), leading to T‑cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape compared with single-antigen CARs.
YES
DIRECT
CAR‑T cells use the APRIL/BAFF ligand domain to bind TACI, triggering CAR signaling and T‑cell cytolytic activity that kills TACI‑expressing cells via perforin/granzyme (and death‑receptor) pathways.
Autologous, lentiviral-engineered chimeric antigen receptor T-cell therapy with a bicephalic APRIL/BAFF ligand domain enabling dual recognition of BCMA and TACI (and possibly BAFF-R) on malignant plasma cells to trigger T-cell activation and cytotoxicity.
Autologous T cells are lentivirally engineered to express a chimeric antigen receptor with a bicephalic APRIL/BAFF ligand domain that binds BCMA and TACI (and possibly BAFF-R) on malignant plasma cells. Receptor engagement activates CAR signaling (CD3ζ with costimulation), leading to T‑cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape compared with single-antigen CARs.
YES
DIRECT
CAR-T cells bind BAFF-R via the BAFF ligand domain of the bicephalic CAR, triggering CD3ζ costimulatory signaling and T-cell–mediated lysis through perforin/granzyme release.