Off-the-shelf allogeneic anti-EGFR–conjugated gamma delta T-cell therapy; healthy-donor γδ T cells conjugated to an anti-EGFR antibody to redirect cytotoxicity toward EGFR-expressing tumor cells; mediates killing via T-cell effector functions.
Off-the-shelf allogeneic gamma delta (gdT) T cells chemically conjugated to an anti-EGFR antibody; the antibody directs the gdT cells to EGFR-expressing tumor cells, enabling MHC-independent recognition and T-cell effector–mediated cytotoxicity (perforin/granzyme release and cytokine production).
Anti-EGFR–conjugated gamma delta T cells bind EGFR on tumor cells and kill them via T-cell effector functions (immune synapse with perforin/granzyme-mediated cytolysis and cytokine release), MHC-independent.
Autologous gene-modified T cells expressing a CD19-directed chimeric antigen receptor to eliminate CD19+ B cells and reduce autoantibody production.
Autologous T cells are engineered to express a CD19-directed chimeric antigen receptor, enabling them to recognize and kill CD19+ B-lineage cells via cytotoxic mechanisms (e.g., perforin/granzyme and cytokine-mediated killing). This depletes autoreactive B cells, reduces autoantibody production, and aims to reset humoral immunity.
Anti-CD19 CAR T cells recognize CD19 and directly lyse target cells via T-cell cytotoxic mechanisms (perforin/granzyme and death-receptor pathways).
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 recognize phosphoantigen-induced BTN2A1/BTN3A1 on target cells via their TCR, activating perforin/granzyme-mediated cytotoxicity (with cytokine release).
Autologous gene-modified T cells expressing chimeric antigen receptors targeting CD19 and BCMA to deplete B cells and plasmablasts/plasma cells.
Autologous T cells engineered to express dual chimeric antigen receptors targeting CD19 and BCMA. Upon antigen engagement, the CAR T cells become activated and lyse CD19+ B cells and BCMA+ plasmablasts/plasma cells (via cytotoxic pathways and cytokine release), depleting autoreactive B-lineage compartments to reduce autoantibody production and reset humoral immunity.
CD19-directed CAR T cells bind CD19 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis and apoptosis (and Fas/FasL), with supportive cytokine effects.
Autologous gene-modified T cells expressing chimeric antigen receptors targeting CD19 and BCMA to deplete B cells and plasmablasts/plasma cells.
Autologous T cells engineered to express dual chimeric antigen receptors targeting CD19 and BCMA. Upon antigen engagement, the CAR T cells become activated and lyse CD19+ B cells and BCMA+ plasmablasts/plasma cells (via cytotoxic pathways and cytokine release), depleting autoreactive B-lineage compartments to reduce autoantibody production and reset humoral immunity.
BCMA-specific CAR T cells bind BCMA on plasmablasts/plasma cells, become activated, and kill targets via perforin/granzyme-mediated cytolysis and apoptosis (and Fas–FasL), with contributory cytokine-mediated effects.