Autologous T cells genetically modified to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on plasmablasts/plasma cells to eliminate antibody-secreting cells and modulate autoimmunity.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes BCMA (TNFRSF17) on plasmablasts and plasma cells. Upon antigen binding, CAR signaling activates the T cells to kill BCMA+ cells via cytotoxic effector functions and cytokine release, depleting antibody-secreting cells and reducing pathogenic autoantibodies to modulate autoimmunity.
YES
DIRECT
CAR recognition of BCMA activates the engineered T cells to kill BCMA+ cells via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with supportive cytokine effects.
Autologous CAR T cells targeting CD19 on B-lineage cells (naive, memory, some plasmablasts) to deplete autoreactive B cells and reduce antigen presentation and autoantibody production.
Autologous T cells are genetically modified to express a chimeric antigen receptor targeting CD19; upon binding CD19 on B-lineage cells (naive, memory, some plasmablasts), CAR signaling activates cytotoxic pathways (perforin/granzyme, death receptors) to deplete B cells, thereby reducing antigen presentation and autoantibody production and helping reset dysregulated humoral immunity.
YES
DIRECT
CD19 CAR T cells bind CD19 on B-lineage cells; CAR signaling triggers perforin/granzyme release and death-receptor pathways (e.g., Fas/FasL), causing apoptosis/lysis of the target cells.
Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.
Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.
YES
DIRECT
NKG2D CAR–NK cells bind MICA on target cells and signal via DAP10/CD3ζ to activate NK degranulation, releasing perforin and granzymes that induce cytolysis/apoptosis.
Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.
Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.
YES
DIRECT
NKG2D CAR on NK cells binds MICB on target cells, activating DAP10/CD3ζ signaling and NK degranulation with perforin/granzyme-mediated lysis.
Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.
Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.
YES
DIRECT
NKG2D CAR on NK cells binds ULBP1 on target cells and signals via DAP10/CD3ζ, triggering NK degranulation (perforin/granzymes) and death receptor pathways to kill the ULBP1+ cells.