CD20×CD3 bispecific T-cell–engaging IgG monoclonal antibody that redirects T cells to lyse CD20-positive B cells, inducing T-cell activation and cytokine release.
CD20×CD3 bispecific IgG antibody that binds CD3 on T cells and CD20 on B cells, crosslinking T cells to CD20-positive malignant B cells to activate cytotoxic T-lymphocyte responses and cytokine release, resulting in targeted lysis of the B cells.
NO
INDIRECT
CD3 engagement activates and redirects T cells; these T cells then kill CD20-positive B cells via perforin/granzyme-mediated cytotoxicity. CD3ε-expressing T cells are not targeted for killing.
Type I anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity and ADCC.
Type I anti‑CD20 chimeric monoclonal antibody that binds CD20 on B cells and depletes them primarily via complement‑dependent cytotoxicity (CDC) and antibody‑dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), leading to elimination of CD20‑positive B cells.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC by NK cells and ADCP by macrophages), leading to lysis/clearance of CD20+ cells.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.