Autologous, ex vivo–expanded tumor-reactive T cells used for adoptive cell therapy to recognize patient-specific tumor antigens and kill cancer cells.
Autologous tumor-infiltrating T cells expanded ex vivo are reinfused to target cancer via their native TCRs, recognizing patient-specific peptide–MHC tumor antigens and killing tumor cells through cytotoxic granule release and cytokine-mediated immune activation; lymphodepletion and IL-2 support engraftment and persistence.
Autologous TILs use their native TCRs to recognize the tumor neoantigen peptide on HLA class II and directly kill the presenting cell via perforin/granzyme release and Fas–FasL–mediated apoptosis, aided by cytotoxic cytokines (e.g., IFN-γ, TNF).
Autologous, ex vivo–expanded tumor-reactive T cells used for adoptive cell therapy to recognize patient-specific tumor antigens and kill cancer cells.
Autologous tumor-infiltrating T cells expanded ex vivo are reinfused to target cancer via their native TCRs, recognizing patient-specific peptide–MHC tumor antigens and killing tumor cells through cytotoxic granule release and cytokine-mediated immune activation; lymphodepletion and IL-2 support engraftment and persistence.
TILs recognize the tumor-associated peptide presented by HLA class II via their native TCRs (CD4+ T cells) and kill the presenting cells through perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis.
Ex vivo engineered/expanded autologous T cells administered intravenously for antigen-directed adoptive cell therapy. These cells recognize a tumor-associated antigen on GI cancers (esophageal, gastric, pancreatic, colorectal) and mediate cytotoxic killing and cytokine-driven immune activation; in vivo expansion and persistence are assessed.
Autologous T cells engineered ex vivo to express a chimeric antigen receptor that recognizes a tumor‑associated antigen on gastrointestinal tumor cells. Upon antigen engagement, CAR signaling (CD3ζ with co‑stimulatory domains) activates the T cells to mediate targeted cytotoxic killing and cytokine release, with in vivo expansion and persistence supporting ongoing anti‑tumor activity.
CAR T cells bind the tumor-associated antigen, form an immune synapse, and kill target cells via perforin/granzyme-mediated cytolysis and apoptosis (Fas–FasL), with cytokine release.
Type II, glycoengineered anti-CD20 monoclonal antibody that induces direct B-cell death and enhances antibody-dependent cellular cytotoxicity.
Type II, glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa engagement from afucosylated Fc glycans, drives potent antibody-dependent cellular cytotoxicity and phagocytosis, and induces direct, caspase-independent B‑cell death, leading to B‑cell depletion.
Obinutuzumab binds CD20 on B cells, inducing direct caspase-independent cell death and engaging FcγRIIIa on effector cells to drive ADCC and phagocytosis (with some complement activity), depleting CD20+ cells.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity and Fc-mediated antibody-dependent cellular cytotoxicity/phagocytosis, leading to apoptosis of targeted B cells.
Rituximab binds CD20 on B cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated ADCC/antibody-dependent phagocytosis; crosslinking can also trigger apoptosis.