Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
YES
INDIRECT
Antigen-specific CTLs recognize peptide–MHC via the TCR and then deliver a lethal hit; FasL on CTLs engages Fas (CD95) on the target to trigger extrinsic apoptosis (caspase-8), with perforin/granzyme also contributing. Fas is an effector receptor, not the recognition target.
Intravenous humanized anti-HER2 IgG1 monoclonal antibody that inhibits HER2 receptor signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); binds the extracellular domain to inhibit HER2-driven signaling and downstream PI3K/AKT and MAPK pathways, and engages Fcγ receptor–bearing immune cells to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on target cells and its Fc engages Fc gamma receptor-bearing effector cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity and lysis; may also contribute via complement activation and HER2 signaling blockade.
Gene-modified natural killer cells engineered to express a chimeric antigen receptor targeting CLL-1 (CLEC12A) for treatment of relapsed/refractory AML; upon CAR engagement of CLL-1, NK cytotoxic mechanisms (perforin/granzyme, cytokines) kill AML blasts and leukemia stem/progenitor cells.
Gene‑modified natural killer cells expressing a CAR that recognizes CLL‑1 (CLEC12A) on AML blasts and leukemia stem/progenitor cells; CAR engagement activates NK cell signaling leading to degranulation and cytotoxic killing via perforin/granzyme and cytokine secretion, with relative sparing of normal hematopoietic stem cells.
YES
DIRECT
CAR-engineered NK cells bind CLEC12A (CLL-1) and, upon CAR engagement, directly kill target cells via NK degranulation with perforin/granzyme-mediated apoptosis and cytotoxic cytokine release.
HER2-directed antibody–drug conjugate consisting of an anti-HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; may also induce ADCC and immunogenic cell death.
HER2-directed antibody–drug conjugate in which an anti-HER2 monoclonal antibody delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells. After binding and internalization, MMAE is released to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; the antibody component may also mediate ADCC and promote immunogenic cell death.
YES
DIRECT
The HER2-targeted ADC binds HER2, is internalized, and releases MMAE that inhibits tubulin polymerization, causing mitotic arrest and apoptosis; the antibody Fc can also mediate ADCC.
HER2-directed antibody–drug conjugate consisting of an anti-HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; may also induce ADCC and immunogenic cell death.
HER2-directed antibody–drug conjugate in which an anti-HER2 monoclonal antibody delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells. After binding and internalization, MMAE is released to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; the antibody component may also mediate ADCC and promote immunogenic cell death.
NO
INDIRECT
The ADC binds HER2, is internalized, and releases MMAE, which binds the vinca domain of beta‑tubulin to block microtubule polymerization, causing mitotic arrest and apoptosis. Beta‑tubulin is the payload’s intracellular target, not the antigen used for targeting.