Autologous (or donor-derived) T cells genetically modified to express an anti-CD19 chimeric antigen receptor that binds CD19 on B-lineage cells and activates T-cell cytotoxicity to eliminate CD19+ leukemic blasts; induces B-cell aplasia.
Autologous or donor-derived T cells are engineered to express an anti‑CD19 chimeric antigen receptor. Binding to CD19 on B‑lineage cells activates CAR signaling (CD3ζ with costimulatory domains), driving T‑cell proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxicity to eradicate CD19+ leukemic blasts, resulting in on‑target B‑cell aplasia.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and apoptosis), leading to on-target B-cell depletion.
Autologous whole-tumor cell vaccine designed to prime and expand neoantigen-specific T-cell responses in newly diagnosed GBM.
Autologous T cells are primed in vivo by a personalized whole-tumor cell vaccine to generate neoantigen-reactive clones, then collected by leukapheresis, activated and expanded ex vivo, and reinfused to recognize patient-specific neoantigens on GBM cells and kill them via TCR-mediated cytotoxic activity; low-dose IL-2 supports T-cell survival and proliferation.
YES
DIRECT
Adoptively transferred neoantigen-specific T cells recognize the patient-specific peptide–MHC I via their TCR and kill target cells through perforin/granzyme release and Fas/FasL-mediated apoptosis.
Anti-HER2 monoclonal antibody that blocks HER2 signaling and induces antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody against HER2 that binds the receptor’s extracellular domain, inhibits HER2-driven signaling/heterodimerization, and engages Fcγ receptors to trigger antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells), inducing antibody-dependent cellular cytotoxicity (ADCC); complement activation may also contribute.
Autologous whole-tumor cell vaccine designed to prime and expand neoantigen-specific T-cell responses in newly diagnosed GBM.
Autologous T cells are primed in vivo by a personalized whole-tumor cell vaccine to generate neoantigen-reactive clones, then collected by leukapheresis, activated and expanded ex vivo, and reinfused to recognize patient-specific neoantigens on GBM cells and kill them via TCR-mediated cytotoxic activity; low-dose IL-2 supports T-cell survival and proliferation.
YES
DIRECT
Adoptively transferred neoantigen-specific T cells recognize the patient-specific peptide–MHC II via their TCR and directly kill target cells through perforin/granzyme release and Fas–FasL-mediated apoptosis.
Patient-derived T lymphocytes activated and expanded ex vivo and reinfused to mediate anti-tumor cytotoxicity via TCR recognition of tumor neoantigens.
Autologous patient T lymphocytes are activated and expanded ex vivo to enrich neoantigen-specific TCR clones. Upon reinfusion, they recognize patient-specific tumor neoantigens presented on HLA and kill tumor cells via TCR-mediated cytotoxicity (perforin/granzyme and cytokine release). No genetic engineering is involved.
YES
DIRECT
Neoantigen-specific TCRs on the reinfused autologous T cells recognize the peptide–HLA class I complex and directly kill target cells via cytotoxic T cell mechanisms (perforin/granzyme-mediated apoptosis, plus Fas–FasL).