Allogeneic engineered T cells transduced ex vivo with a lentiviral vector to express an Epstein–Barr virus–specific T-cell receptor (HLA-A*02:01/11:01/24:02–restricted). Administered at 1×10^6–1×10^8 cells/kg for adoptive cellular immunotherapy to recognize EBV-derived peptides on MHC I and eliminate EBV-infected cells in EBV-associated HLH or persistent EBV infection.
Allogeneic T cells are engineered ex vivo with a lentiviral vector to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor. Upon recognition of EBV-derived peptides presented on MHC class I of infected host cells, the introduced TCR triggers T-cell activation and cytotoxic effector functions (perforin/granzyme, Fas–FasL) and cytokine release, leading to targeted elimination of EBV-infected cells and reduction of EBV-driven inflammation (e.g., in EBV-HLH or persistent EBV infection).
TCR-engineered T cells recognize EBV-derived peptide presented by HLA-A*24:02 on target cells and induce cytotoxicity via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous anti-BCMA chimeric antigen receptor (CAR) T-cell therapy: patient T lymphocytes are genetically engineered to express a CAR targeting BCMA and infused intravenously (3+3 dose escalation, up to 6×10^6 CAR-T cells/kg). CAR engagement activates T-cell cytotoxicity (degranulation, cytokine release, proliferation) to eliminate BCMA-positive myeloma cells. The construct includes EGFR expression as a built-in safety/control feature.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor targeting BCMA. Upon binding BCMA on malignant plasma cells, CAR signaling (CD3 zeta with costimulatory domains) activates T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate BCMA-positive cells. The construct co-expresses EGFR as a safety/control feature.
Anti-BCMA CAR-T cells bind BCMA on target cells, triggering CAR signaling and T-cell degranulation to kill BCMA+ cells via perforin/granzyme-mediated cytotoxicity.
Anti-CD38 monoclonal antibody that targets malignant plasma cells; mediates ADCC, CDC, ADCP, and immune modulation.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, inducing immune effector–mediated killing (ADCC, CDC) and phagocytosis (ADCP), and depleting CD38-positive immunosuppressive cells (Tregs, B cells, MDSCs) to enhance antitumor immunity.
Anti-CD38 IgG1 binds CD38 on target cells and recruits immune effectors via its Fc domain, causing NK cell–mediated ADCC, macrophage-mediated ADCP, and complement-dependent cytotoxicity (CDC); may also induce apoptosis upon crosslinking.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
Vγ9Vδ2 T cells expressing CD16 (FcγRIIIa) bind IgG Fc on opsonized tumor cells, triggering ADCC and perforin/granzyme-mediated killing.
Bispecific T-cell engager antibody targeting BCMA on plasma cells and CD3 on T cells to redirect T-cell cytotoxicity.
Bispecific humanized monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, cross-linking them to form an immune synapse and redirect T-cell cytotoxicity, leading to T-cell activation and lysis of BCMA-expressing malignant plasma cells.
Teclistamab binds BCMA on target cells and CD3 on T cells, forming an immune synapse that redirects T-cell killing via perforin/granzyme-mediated lysis of BCMA-expressing cells.