Autologous CD8+/CD4+ T cells expanded ex vivo from the patient's tumor to recognize tumor antigens via native TCRs; administered as adoptive cell therapy.
Autologous tumor-infiltrating CD8+/CD4+ T cells expanded ex vivo are reinfused to restore large numbers of tumor-reactive lymphocytes. Using native TCRs, they recognize patient-specific tumor antigens presented on MHC, traffic to tumor sites, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion. Lymphodepletion and IL-2 support enhance in vivo expansion and persistence.
CD4+ TILs recognize tumor-derived peptide–HLA-DR via their native TCRs and directly kill the presenting cell through perforin/granzyme release and Fas–FasL apoptosis, with IFN-γ/TNF-α aiding cytotoxicity.
Autologous CD8+/CD4+ T cells expanded ex vivo from the patient's tumor to recognize tumor antigens via native TCRs; administered as adoptive cell therapy.
Autologous tumor-infiltrating CD8+/CD4+ T cells expanded ex vivo are reinfused to restore large numbers of tumor-reactive lymphocytes. Using native TCRs, they recognize patient-specific tumor antigens presented on MHC, traffic to tumor sites, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion. Lymphodepletion and IL-2 support enhance in vivo expansion and persistence.
TILs use native TCRs (CD4+ T cells) to recognize tumor-derived peptides presented on HLA-DP (MHC II) and directly lyse target cells via perforin/granzyme and Fas–FasL pathways, with cytokines (IFN-γ/TNFα) augmenting cytotoxicity.
Autologous CD8+/CD4+ T cells expanded ex vivo from the patient's tumor to recognize tumor antigens via native TCRs; administered as adoptive cell therapy.
Autologous tumor-infiltrating CD8+/CD4+ T cells expanded ex vivo are reinfused to restore large numbers of tumor-reactive lymphocytes. Using native TCRs, they recognize patient-specific tumor antigens presented on MHC, traffic to tumor sites, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion. Lymphodepletion and IL-2 support enhance in vivo expansion and persistence.
CD4+ TILs recognize tumor-derived peptide presented by HLA-DQ via their native TCR and directly kill the presenting cell through perforin/granzyme release (and Fas–FasL pathways).
An intravenously administered IgM bispecific T-cell–engaging antibody that binds CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity and deplete pathogenic B cells.
Imvotamab is an IgM bispecific antibody that binds CD20 on B cells and CD3 on T cells, forming an immune synapse to redirect T‑cell cytotoxicity and deplete CD20+ B cells; its multivalent IgM format enhances binding to low‑CD20 cells and adds complement‑dependent cytotoxicity (CDC) while potentially reducing cytokine release versus IgG bispecifics.
Binds CD20 on B cells and CD3 on T cells to form an immune synapse, causing T‑cell perforin/granzyme‑mediated killing; IgM format also activates complement for CDC against CD20+ cells.
Autologous, gene-modified T cells engineered to express chimeric antigen receptors that bind surface antigens on malignant B cells in B-cell non-Hodgkin lymphoma, enabling HLA-independent T-cell activation, cytokine release, and cytotoxic tumor cell killing; administered per routine care in this observational study.
Autologous T cells are gene-engineered to express chimeric antigen receptors that bind tumor surface antigens (e.g., CD19 on B cells), enabling HLA-independent recognition; CAR signaling activates T cells to proliferate, release cytokines, and exert cytotoxic killing of malignant cells.
CAR T cells recognize CD19 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytolysis and apoptosis (and Fas/FasL signaling).