Autologous ex vivo-expanded T cells isolated from the patient’s tumor, infused to provide tumor-specific cytotoxic CD8+/CD4+ T cells for adoptive cellular immunotherapy.
Autologous tumor-resident T cells isolated from the patient’s tumor are expanded ex vivo and reinfused to provide polyclonal, tumor‑antigen–specific CD8+/CD4+ T cells. These cells recognize tumor antigens via their native TCRs in an MHC-restricted manner and mediate cytotoxicity (perforin/granzyme) and cytokine release to eliminate tumor cells; they are not genetically engineered.
TILs recognize the patient-specific neoantigen peptide presented on HLA class II via their native TCRs and directly kill the presenting tumor cell through perforin/granzyme release and/or Fas–FasL–mediated apoptosis.
Autologous ex vivo-expanded T cells isolated from the patient’s tumor, infused to provide tumor-specific cytotoxic CD8+/CD4+ T cells for adoptive cellular immunotherapy.
Autologous tumor-resident T cells isolated from the patient’s tumor are expanded ex vivo and reinfused to provide polyclonal, tumor‑antigen–specific CD8+/CD4+ T cells. These cells recognize tumor antigens via their native TCRs in an MHC-restricted manner and mediate cytotoxicity (perforin/granzyme) and cytokine release to eliminate tumor cells; they are not genetically engineered.
TILs use native TCRs to recognize the tumor-associated peptide on HLA class II and directly kill antigen-bearing cells via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Fully human bispecific IgG4 monoclonal antibody intended to engage immune effectors to kill malignant B cells (specific targets not stated).
Fully human bispecific IgG4 antibody that binds CD3 on T cells and CD19 on B cells, physically redirecting cytotoxic T lymphocytes to CD19+ malignant B cells to induce perforin/granzyme-mediated killing. The fixed-light-chain arm weakly activates CD3, while the heavy-chain-only arm binds CD19 with high affinity, enabling MHC-independent T-cell engagement and tumor cell lysis.
Bispecific antibody bridges CD3 on T cells to CD19 on target cells, redirecting CTLs to form an immune synapse and kill CD19+ cells via perforin/granzyme-mediated cytolysis.
Chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via ADCC, complement activation (CDC), and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Rituximab binds CD20 on B cells and engages immune effectors via its Fc to mediate ADCC; it also activates complement for CDC and can induce apoptosis upon CD20 crosslinking, leading to killing of CD20+ cells.
Anti-HER2 humanized monoclonal antibody that binds ERBB2 (HER2) to inhibit signaling and mediate antibody-dependent cellular cytotoxicity.
Humanized anti-HER2 monoclonal antibody that binds ERBB2 (HER2) on tumor cells, blocks HER2 signaling and growth, and mediates antibody-dependent cell-mediated cytotoxicity via Fc receptor–bearing immune cells.
Trastuzumab binds HER2 on target cells and engages Fcγ receptor–bearing immune cells (e.g., NK cells, macrophages) to mediate antibody-dependent cellular cytotoxicity; may also activate complement and induce apoptosis.