Autologous dendritic cell cancer vaccine engineered to present WT1 antigens via MHC I/II and surface-display the IL-15/IL-15Rα complex to enhance CD8+ T-cell and NK-cell activation, proliferation, cytotoxicity, and memory.
Autologous dendritic cells engineered to present WT1 antigens on MHC I/II and to surface-transpresent the IL-15/IL-15Ralpha complex, thereby priming and expanding WT1-specific CD8+ and CD4+ T cells and enhancing CD8+ T-cell and NK-cell activation, proliferation, cytotoxicity, survival, and memory via IL-15 signaling.
NO
INDIRECT
IL-15 is used as a stimulatory signal (transpresented by the vaccine DCs) to expand/activate CD8+ T and NK cells; these effectors kill WT1-expressing tumor cells via perforin/granzyme-mediated cytotoxicity, not IL-15–expressing cells.
Autologous dendritic cell cancer vaccine engineered to present WT1 antigens via MHC I/II and surface-display the IL-15/IL-15Rα complex to enhance CD8+ T-cell and NK-cell activation, proliferation, cytotoxicity, and memory.
Autologous dendritic cells engineered to present WT1 antigens on MHC I/II and to surface-transpresent the IL-15/IL-15Ralpha complex, thereby priming and expanding WT1-specific CD8+ and CD4+ T cells and enhancing CD8+ T-cell and NK-cell activation, proliferation, cytotoxicity, survival, and memory via IL-15 signaling.
NO
INDIRECT
CD122+ T and NK cells are stimulated by IL-15/IL-15Rα transpresentation from the dendritic-cell vaccine, expanding and enhancing their cytotoxicity; these effectors then kill WT1-expressing tumor cells, not the CD122-expressing cells.
Autologous dendritic cell cancer vaccine engineered to present WT1 antigens via MHC I/II and surface-display the IL-15/IL-15Rα complex to enhance CD8+ T-cell and NK-cell activation, proliferation, cytotoxicity, and memory.
Autologous dendritic cells engineered to present WT1 antigens on MHC I/II and to surface-transpresent the IL-15/IL-15Ralpha complex, thereby priming and expanding WT1-specific CD8+ and CD4+ T cells and enhancing CD8+ T-cell and NK-cell activation, proliferation, cytotoxicity, survival, and memory via IL-15 signaling.
NO
INDIRECT
The vaccine trans-presents IL-15/IL-15Ralpha to CD132/CD122 on T and NK cells, activating and expanding them; these effectors then kill WT1-expressing tumor cells via CTL and NK cytotoxicity. CD132+ cells are not targeted for killing.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (Fc-mediated engagement of NK cells/macrophages), complement-dependent cytotoxicity, and can trigger apoptosis upon CD20 crosslinking.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy manufactured via SIN lentiviral transduction of CD4/CD8 T cells; single IV dose (1×10^6/kg). Designed to deplete CD19+ B cells and plasmablasts to reduce autoantibody-driven inflammation.
Autologous T cells are engineered via lentiviral transduction to express an anti-CD19 chimeric antigen receptor that recognizes CD19 on B-lineage cells. Upon engagement, CAR T cells mediate cytotoxic killing (e.g., perforin/granzyme) and depletion of CD19+ B cells and plasmablasts, leading to reduced autoantibody production and attenuation of B cell–driven inflammation.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on B-lineage cells and directly kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, with possible Fas–FasL contributions).