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.
YES
DIRECT
Vγ9Vδ2 T cells sense phosphoantigen-induced BTN3A1/BTN2A1 on target cells via their TCR, triggering activation and perforin/granzyme-mediated cytolysis (with NKG2D co-stimulation).
Autologous TCR-engineered T-cell therapy targeting KRAS G12D presented by HLA-A*11:01 or HLA-A*11:02; infused cells recognize the KRAS G12D peptide–HLA complex on tumor cells and mediate cytotoxic killing.
Autologous T cells are genetically engineered to express a T-cell receptor that recognizes the KRAS G12D peptide presented by HLA-A*11:01 or HLA-A*11:02 on tumor cells. Upon antigen recognition, the engineered T cells become activated and mediate cytotoxic killing of KRAS G12D–positive tumor cells via TCR signaling, cytokine release, and perforin/granzyme pathways.
YES
DIRECT
Engineered TCR T cells recognize the KRAS G12D peptide–HLA-A*11:01 complex and kill target cells via TCR-activated cytotoxic pathways, primarily perforin/granzyme-mediated apoptosis (with supportive cytokine effects).
Autologous TCR-engineered T-cell therapy targeting KRAS G12D presented by HLA-A*11:01 or HLA-A*11:02; infused cells recognize the KRAS G12D peptide–HLA complex on tumor cells and mediate cytotoxic killing.
Autologous T cells are genetically engineered to express a T-cell receptor that recognizes the KRAS G12D peptide presented by HLA-A*11:01 or HLA-A*11:02 on tumor cells. Upon antigen recognition, the engineered T cells become activated and mediate cytotoxic killing of KRAS G12D–positive tumor cells via TCR signaling, cytokine release, and perforin/granzyme pathways.
YES
DIRECT
Engineered TCR T cells recognize the KRAS G12D–HLA-A*11:02 complex and directly lyse target cells via TCR activation leading to perforin/granzyme-mediated apoptosis (with supportive cytokine effects).
Autologous, gene-modified T cells engineered to express a chimeric antigen receptor that binds CD19; administered as a single IV infusion to activate cytotoxic T-cell killing of CD19+ B-lineage cells, leading to B-cell depletion and reduced autoantibody production.
Autologous T cells are gene-modified to express a chimeric antigen receptor that binds CD19 on B-lineage cells. Upon engagement, CAR-T cells activate and mediate cytotoxic killing (perforin/granzyme and cytokines), leading to profound depletion of CD19+ B cells/plasmablasts, reduction of autoantibody production, and functional resetting of humoral immunity.
YES
DIRECT
CD19 CAR-T cells bind CD19 on B-lineage cells, form an immune synapse, and kill targets via perforin/granzyme-mediated cytolysis (and death-receptor pathways), depleting CD19+ cells.
Autologous T cells engineered ex vivo to express a chimeric antigen receptor targeting BCMA (TNFRSF17); upon BCMA engagement, CAR signaling activates T-cell cytotoxicity and cytokine release to eliminate BCMA-expressing myeloma cells.
Autologous T cells are engineered to express a chimeric antigen receptor that binds BCMA (TNFRSF17); upon BCMA engagement on myeloma cells, CAR signaling activates T-cell cytotoxicity and cytokine release, leading to perforin/granzyme-mediated lysis of BCMA-expressing cells.
YES
DIRECT
BCMA-specific CAR T cells engage BCMA on target cells, become activated, and kill via immunologic synapse with perforin/granzyme release (and Fas–FasL), inducing apoptosis/lysis.