Autologous TH1-polarizing dendritic cell vaccine loaded with patient tumor lysate and mRNA-encoded antigens to enhance antigen presentation (MHC I/II) and prime CD8+ cytotoxic T cells and CD4+ TH1 responses, boosting IFN-γ–mediated antitumor immunity.
Autologous TH1-polarized dendritic cells are loaded ex vivo with patient tumor lysate and mRNA-encoded tumor antigens. The DCs process/translate antigens and present peptides on MHC class I and II to cross-prime tumor-specific CD8+ cytotoxic T cells and activate CD4+ TH1 cells, enhancing IFN-γ–mediated antitumor immunity.
YES
INDIRECT
The DC vaccine primes tumor-specific CD8+ T cells that recognize the MHC I–presented tumor peptides and kill antigen-expressing cells via perforin/granzyme (and Fas–FasL) cytotoxicity, augmented by TH1/IFN-γ signaling.
Autologous TH1-polarizing dendritic cell vaccine loaded with patient tumor lysate and mRNA-encoded antigens to enhance antigen presentation (MHC I/II) and prime CD8+ cytotoxic T cells and CD4+ TH1 responses, boosting IFN-γ–mediated antitumor immunity.
Autologous TH1-polarized dendritic cells are loaded ex vivo with patient tumor lysate and mRNA-encoded tumor antigens. The DCs process/translate antigens and present peptides on MHC class I and II to cross-prime tumor-specific CD8+ cytotoxic T cells and activate CD4+ TH1 cells, enhancing IFN-γ–mediated antitumor immunity.
YES
INDIRECT
Vaccine DCs present tumor-lysate MHC II peptides to activate TH1 cells, which provide help for tumor-specific CD8+ CTLs. These CTLs recognize corresponding antigens on tumor cells (via MHC I) and kill them via perforin/granzyme and Fas–FasL pathways; the vaccine does not directly kill target-expressing cells.
Human IgG1 monoclonal antibody immune checkpoint inhibitor that binds PD-L1, blocking its interaction with PD-1 and B7.1 to restore T-cell antitumor activity; retains an intact Fc region enabling ADCC and engagement of NK cells.
Human IgG1 monoclonal antibody that binds PD-L1, blocking its interaction with PD-1 and B7.1 to inhibit PD-1 signaling and restore T-cell antitumor activity; the intact Fc region engages Fc receptors to mediate antibody-dependent cellular cytotoxicity against PD-L1-expressing cells.
YES
DIRECT
Avelumab binds PD-L1 on target cells and, via its intact IgG1 Fc, engages Fc gamma receptors (e.g., CD16) on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), killing PD-L1–expressing cells; it also blocks PD-1/PD-L1 to restore T-cell activity (indirect).
Human IgG1 monoclonal antibody immune checkpoint inhibitor that binds PD-L1, blocking its interaction with PD-1 and B7.1 to restore T-cell antitumor activity; retains an intact Fc region enabling ADCC and engagement of NK cells.
Human IgG1 monoclonal antibody that binds PD-L1, blocking its interaction with PD-1 and B7.1 to inhibit PD-1 signaling and restore T-cell antitumor activity; the intact Fc region engages Fc receptors to mediate antibody-dependent cellular cytotoxicity against PD-L1-expressing cells.
NO
INDIRECT
Avelumab binds PD-L1 on target cells; its Fc engages CD16a (FcγRIIIa) on NK cells to trigger ADCC against PD-L1-expressing cells. CD16a-expressing cells serve as effectors and are not killed by the drug.
HER2-targeted antibody-drug conjugate (Enhertu, T-DXd) that delivers a topoisomerase I inhibitor (DXd) to HER2-expressing tumor cells, causing DNA damage and bystander killing.
HER2-targeted monoclonal antibody (trastuzumab) delivers a membrane-permeable topoisomerase I inhibitor payload (DXd) to HER2-expressing tumor cells. After HER2 binding and internalization, DXd inhibits Top1, causing DNA damage, replication blockade, and apoptosis; additional effects include bystander killing and antibody-dependent cell-mediated cytotoxicity (ADCC).
YES
DIRECT
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor payload, causing DNA damage and apoptosis in HER2+ cells; it can also mediate ADCC and bystander killing.