Intravenous anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells, causing B-cell depletion through antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptosis.
Rituximab binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (through FcγR-bearing effector cells), complement-dependent cytotoxicity, and can trigger direct apoptosis upon CD20 cross-linking.
Autologous adoptive cell therapy of neoantigen-selected, tumor‑reactive tumor‑infiltrating lymphocytes (TILs) expanded ex vivo and infused after lymphodepletion with IL‑2 support.
Autologous tumor-infiltrating lymphocytes selected for neoantigen-specific tumor reactivity are expanded ex vivo and reinfused after lymphodepletion. These T cells recognize patient-specific tumor neoantigens via their native TCRs in an MHC-restricted manner and mediate direct cytotoxic killing and cytokine-driven anti-tumor responses; IL-2 support promotes their engraftment, survival, and expansion.
Neoantigen-specific TILs recognize the mutant peptide–HLA class I complex via their native TCRs and directly kill target cells through perforin/granzyme cytolysis and Fas–FasL engagement; IL-2 supports T-cell expansion.
Autologous adoptive cell therapy of neoantigen-selected, tumor‑reactive tumor‑infiltrating lymphocytes (TILs) expanded ex vivo and infused after lymphodepletion with IL‑2 support.
Autologous tumor-infiltrating lymphocytes selected for neoantigen-specific tumor reactivity are expanded ex vivo and reinfused after lymphodepletion. These T cells recognize patient-specific tumor neoantigens via their native TCRs in an MHC-restricted manner and mediate direct cytotoxic killing and cytokine-driven anti-tumor responses; IL-2 support promotes their engraftment, survival, and expansion.
Neoantigen-specific TILs recognize the mutant peptide–HLA class II complex via their native TCRs and directly kill the presenting cell through perforin/granzyme release and death-receptor (e.g., Fas/FasL) pathways, with cytokines augmenting the response.
Patient-derived T cells genetically engineered to express a chimeric antigen receptor targeting CD1a; upon infusion, CAR signaling (CD3ζ with costimulation) activates cytotoxicity and proliferation to eliminate CD1a-positive T-ALL/LBL cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CD1a. Engagement of CD1a on T-ALL/LBL cells triggers CAR signaling (CD3zeta with costimulatory domains), activating proliferation and cytotoxic effector functions (perforin/granzyme release and cytokine secretion) to selectively kill CD1a-positive tumor cells.
Anti-CD1a CAR-T cells bind CD1a and, upon CAR activation (CD3ζ with costimulation), kill targets via cytolytic degranulation (perforin/granzymes) and apoptotic/lytic pathways.
Autologous, lentivirally transduced second-generation CAR T-cell therapy (CD4+ and CD8+) targeting B7-H3 (CD276), EGFR806 epitope on EGFR/EGFRvIII, HER2 (ERBB2), and IL13Rα2 via an IL13-zetakine design; administered locoregionally via intraventricular catheter to drive CAR-mediated cytotoxic killing of CNS tumor cells and mitigate antigen escape.
Autologous CD4+/CD8+ T cells are lentivirally engineered to express four second-generation CARs targeting B7-H3 (CD276), the tumor-restricted EGFR806 epitope on EGFR/EGFRvIII, HER2, and IL13Ra2 (via an IL13-zetakine design). Following locoregional intraventricular delivery, CAR engagement drives antigen-specific T-cell activation, cytokine release, and cytotoxic killing of CNS tumor cells, with multi-antigen targeting intended to mitigate antigen escape.
CAR T cells engineered to recognize B7-H3 bind the antigen on tumor cells and induce cytolysis via T-cell effector functions (perforin/granzyme-mediated apoptosis, with possible Fas/FasL signaling).