Autologous adoptive cell therapy using patient-derived tumor-infiltrating T cells expanded ex vivo to recognize and kill cancer cells.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepletion. These unengineered T cells recognize patient-specific tumor antigens via their native TCRs and mediate MHC-restricted cytotoxicity (perforin/granzyme) and cytokine-driven immune responses within the tumor, resulting in direct killing of cancer cells; IL-2 is often provided to support in vivo expansion and persistence.
TILs recognize the neoantigen peptide–HLA class I complex via native TCRs and directly kill target cells through MHC-restricted cytotoxicity (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Autologous adoptive cell therapy using patient-derived tumor-infiltrating T cells expanded ex vivo to recognize and kill cancer cells.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepletion. These unengineered T cells recognize patient-specific tumor antigens via their native TCRs and mediate MHC-restricted cytotoxicity (perforin/granzyme) and cytokine-driven immune responses within the tumor, resulting in direct killing of cancer cells; IL-2 is often provided to support in vivo expansion and persistence.
TILs contain tumor‑reactive CD4+ T cells whose native TCRs recognize the peptide–HLA class II complex on target cells, triggering MHC II–restricted cytotoxicity via perforin/granzyme release and Fas–FasL–mediated apoptosis.
A human IgG1 monoclonal antibody targeting OX40 (CD134) on activated T cells; blocks OX40–OX40L costimulation and can deplete OX40+ T cells to reduce type‑2 inflammation.
Human IgG1 monoclonal antibody that binds OX40 (CD134) on activated T cells, blocking OX40–OX40L costimulatory signaling and, via Fc effector functions, can deplete OX40+ T cells, reducing type‑2 (Th2) inflammation.
After binding OX40 on activated T cells, the IgG1 Fc engages effector mechanisms (ADCC/ADCP and possibly complement), leading to depletion/lysis of OX40+ cells.
Autologous, gene‑modified CD19‑directed CAR T‑cell therapy (CARTEYVA). Patient T cells are engineered to express an anti‑CD19 chimeric antigen receptor with 4‑1BB costimulatory and CD3ζ signaling domains; upon binding CD19 on B‑cell lymphomas, the CAR T cells expand and mediate perforin/granzyme‑dependent cytotoxicity, leading to B‑cell depletion.
Autologous T cells are gene-modified to express an anti-CD19 chimeric antigen receptor with 4-1BB costimulatory and CD3ζ signaling domains; upon binding CD19 on malignant B cells, the CAR T cells activate, expand, and kill targets via perforin/granzyme-mediated cytotoxicity, depleting CD19-positive B-cell lymphomas.
Anti-CD19 CAR T cells bind CD19 on target cells, activate, and kill via perforin/granzyme-mediated cytotoxicity leading to apoptosis/lysis.
Autologous CD19-directed CAR T-cell therapy that redirects T cells to CD19+ B cells to induce cytotoxicity.
Autologous CD19-directed chimeric antigen receptor T-cell therapy. Patient T cells are engineered to express a CAR (with 4-1BB costimulatory and CD3ζ signaling domains) that binds CD19 on B cells, triggering T-cell activation, proliferation, and cytotoxic killing of CD19+ malignant B cells.
CD19-directed CAR T cells bind CD19 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).