Autologous adoptive cell therapy comprising patient-derived tumor-reactive T cells isolated from bladder tumors, expanded ex vivo with IL-2 and anti-CD3 stimulation, and administered intravesically to treat high-grade non-muscle-invasive urothelial carcinoma.
Autologous tumor-infiltrating lymphocytes (TIL) are isolated from the patient’s bladder tumor, activated and expanded ex vivo with IL-2 and anti-CD3, then administered intravesically. These non-engineered T cells recognize tumor antigens via their native TCRs and mediate cytotoxicity (perforin/granzyme) and cytokine release (e.g., IFN-γ), increasing local anti-tumor immunity within the bladder.
TILs recognize tumor antigen peptide–HLA-B complexes via their native TCR and directly kill target cells through immunologic synapse formation and perforin/granzyme-mediated apoptosis (with possible Fas–FasL engagement).
Autologous adoptive cell therapy comprising patient-derived tumor-reactive T cells isolated from bladder tumors, expanded ex vivo with IL-2 and anti-CD3 stimulation, and administered intravesically to treat high-grade non-muscle-invasive urothelial carcinoma.
Autologous tumor-infiltrating lymphocytes (TIL) are isolated from the patient’s bladder tumor, activated and expanded ex vivo with IL-2 and anti-CD3, then administered intravesically. These non-engineered T cells recognize tumor antigens via their native TCRs and mediate cytotoxicity (perforin/granzyme) and cytokine release (e.g., IFN-γ), increasing local anti-tumor immunity within the bladder.
Adoptively transferred TILs recognize tumor antigen peptide–HLA-C complexes via their native TCRs and directly kill the presenting cells through cytotoxic T-cell mechanisms (perforin/granzyme and Fas–FasL).
Intravenous CD20×CD3 bispecific antibody that redirects T cells to kill CD20-positive B cells.
CD20×CD3 bispecific antibody that binds CD3 on T cells and CD20 on B cells to crosslink them, activating T cells to mediate cytotoxic killing of CD20-positive B-cell malignancies.
Glofitamab bridges CD3 on T cells to CD20 on target B cells, activating T cells to form an immunologic synapse and kill CD20+ cells via perforin/granzyme-mediated cytolysis and apoptosis.
Autologous adoptive cell therapy comprising patient-derived tumor-reactive T cells isolated from bladder tumors, expanded ex vivo with IL-2 and anti-CD3 stimulation, and administered intravesically to treat high-grade non-muscle-invasive urothelial carcinoma.
Autologous tumor-infiltrating lymphocytes (TIL) are isolated from the patient’s bladder tumor, activated and expanded ex vivo with IL-2 and anti-CD3, then administered intravesically. These non-engineered T cells recognize tumor antigens via their native TCRs and mediate cytotoxicity (perforin/granzyme) and cytokine release (e.g., IFN-γ), increasing local anti-tumor immunity within the bladder.
TILs recognize the tumor antigen peptide presented by HLA-DR via their native TCRs and directly kill the presenting cells through perforin/granzyme-mediated apoptosis (and Fas-FasL pathways).
Autologous adoptive cell therapy comprising patient-derived tumor-reactive T cells isolated from bladder tumors, expanded ex vivo with IL-2 and anti-CD3 stimulation, and administered intravesically to treat high-grade non-muscle-invasive urothelial carcinoma.
Autologous tumor-infiltrating lymphocytes (TIL) are isolated from the patient’s bladder tumor, activated and expanded ex vivo with IL-2 and anti-CD3, then administered intravesically. These non-engineered T cells recognize tumor antigens via their native TCRs and mediate cytotoxicity (perforin/granzyme) and cytokine release (e.g., IFN-γ), increasing local anti-tumor immunity within the bladder.
TILs recognize the tumor peptide–HLA-DP complex via native TCRs and directly kill target cells through perforin/granzyme release (and Fas–FasL–mediated apoptosis).