Autologous, ex vivo–expanded, multi–tumor-associated antigen (TAA)–specific CD4+ and CD8+ T cells used as adoptive T-cell therapy for relapsed/refractory lymphomas; mediates TCR/HLA-dependent recognition of multiple TAAs to induce cytotoxic killing and helper cytokine support.
Autologous, ex vivo–expanded CD4+ and CD8+ T cells specific for multiple tumor-associated antigens recognize HLA-presented TAAs via their native TCRs, leading to cytotoxic killing (perforin/granzyme) and helper cytokine support; multi-antigen targeting aims to reduce antigen escape.
Autologous T cells recognize HLA-presented PRAME peptides via native TCRs and kill target cells through perforin/granzyme-mediated cytotoxicity (leading to apoptosis).
Autologous, ex vivo–expanded, multi–tumor-associated antigen (TAA)–specific CD4+ and CD8+ T cells used as adoptive T-cell therapy for relapsed/refractory lymphomas; mediates TCR/HLA-dependent recognition of multiple TAAs to induce cytotoxic killing and helper cytokine support.
Autologous, ex vivo–expanded CD4+ and CD8+ T cells specific for multiple tumor-associated antigens recognize HLA-presented TAAs via their native TCRs, leading to cytotoxic killing (perforin/granzyme) and helper cytokine support; multi-antigen targeting aims to reduce antigen escape.
Autologous TAA-specific T cells recognize HLA-presented survivin peptides via native TCRs and directly kill target cells through perforin/granzyme-mediated cytotoxicity (with possible death-receptor signaling).
Autologous, ex vivo–expanded, multi–tumor-associated antigen (TAA)–specific CD4+ and CD8+ T cells used as adoptive T-cell therapy for relapsed/refractory lymphomas; mediates TCR/HLA-dependent recognition of multiple TAAs to induce cytotoxic killing and helper cytokine support.
Autologous, ex vivo–expanded CD4+ and CD8+ T cells specific for multiple tumor-associated antigens recognize HLA-presented TAAs via their native TCRs, leading to cytotoxic killing (perforin/granzyme) and helper cytokine support; multi-antigen targeting aims to reduce antigen escape.
Autologous T cells recognize WT1-derived peptides presented on HLA via their native TCRs and directly lyse target cells through perforin/granzyme-mediated cytotoxicity (with CD4+ helper support).
Autologous, ex vivo–expanded, multi–tumor-associated antigen (TAA)–specific CD4+ and CD8+ T cells used as adoptive T-cell therapy for relapsed/refractory lymphomas; mediates TCR/HLA-dependent recognition of multiple TAAs to induce cytotoxic killing and helper cytokine support.
Autologous, ex vivo–expanded CD4+ and CD8+ T cells specific for multiple tumor-associated antigens recognize HLA-presented TAAs via their native TCRs, leading to cytotoxic killing (perforin/granzyme) and helper cytokine support; multi-antigen targeting aims to reduce antigen escape.
Infused autologous T cells use native TCRs to recognize HLA-presented MAGE-A4 peptides on target cells, triggering cytotoxic T-lymphocyte killing via perforin/granzyme (with possible Fas–FasL) and helper cytokine support.
Autologous, ex vivo–expanded, multi–tumor-associated antigen (TAA)–specific CD4+ and CD8+ T cells used as adoptive T-cell therapy for relapsed/refractory lymphomas; mediates TCR/HLA-dependent recognition of multiple TAAs to induce cytotoxic killing and helper cytokine support.
Autologous, ex vivo–expanded CD4+ and CD8+ T cells specific for multiple tumor-associated antigens recognize HLA-presented TAAs via their native TCRs, leading to cytotoxic killing (perforin/granzyme) and helper cytokine support; multi-antigen targeting aims to reduce antigen escape.
Autologous TAA-specific T cells recognize HLA-presented NY-ESO-1 peptides via native TCRs and kill target cells through perforin/granzyme-mediated cytolysis (with helper cytokine support).