Autologous, gene-modified T cells engineered to express a chimeric antigen receptor targeting CD7; antigen engagement triggers T-cell activation, expansion, cytokine release, and cytolytic killing of CD7+ malignant cells, with on-target effects on normal CD7+ T cells and NK cells.
Autologous T cells genetically modified to express a chimeric antigen receptor targeting CD7. Upon binding CD7 on target cells, CAR signaling activates the T cells, driving expansion, cytokine release, and perforin/granzyme-mediated killing of CD7+ malignant cells, with on-target depletion of normal CD7+ T cells and NK cells.
CAR engagement of CD7 activates the engineered T cells to form a cytolytic synapse and kill CD7+ cells via perforin/granzyme–mediated apoptosis (and potentially death-receptor pathways).
Subcutaneous bispecific IgG antibody (CD3xCD20) that redirects T cells to kill CD20-positive B cells.
Bispecific IgG antibody that binds CD3 on T cells and CD20 on B cells, crosslinking T cells to malignant B cells to activate cytotoxic T-lymphocyte responses and induce perforin/granzyme-mediated killing of CD20-positive cells.
Bispecific antibody links CD3+ T cells to CD20+ cells, activating T-cell cytotoxicity and perforin/granzyme-mediated killing of the CD20-expressing cells.
Adoptive cellular immunotherapy using T cells engineered with chimeric antigen receptors to target B-cell antigens.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes B-cell antigens (e.g., CD19/CD20). Antigen engagement triggers CAR signaling (CD3zeta plus costimulatory domains), leading to T-cell activation, proliferation, cytokine release, and MHC-independent cytotoxic killing of antigen-expressing B cells.
CAR T cells bind CD19 via the CAR, become activated, and kill CD19+ cells through perforin/granzyme-mediated cytolysis and apoptosis (and death-receptor pathways), independent of MHC.
Adoptive cellular immunotherapy using T cells engineered with chimeric antigen receptors to target B-cell antigens.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes B-cell antigens (e.g., CD19/CD20). Antigen engagement triggers CAR signaling (CD3zeta plus costimulatory domains), leading to T-cell activation, proliferation, cytokine release, and MHC-independent cytotoxic killing of antigen-expressing B cells.
CAR T cells recognizing CD20 bind the antigen and, upon CAR signaling, directly lyse CD20+ cells via perforin/granzyme release and death-receptor pathways (MHC-independent).
DLL3xCD3 bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells to redirect and activate cytotoxic T-cell killing.
Bispecific T-cell–engaging antibody that binds DLL3 on tumor cells and CD3 on T cells, forming an immune synapse to activate and redirect cytotoxic T cells to kill DLL3-expressing cancer cells.
DLL3xCD3 T-cell–engaging antibody bridges DLL3 on target cells to CD3 on T cells, forming an immune synapse that activates T cells to release perforin/granzymes and kill DLL3-expressing cells.