Genetically engineered natural killer cells expressing an anti-CD19 chimeric antigen receptor to target and deplete CD19+ B cells via NK cytotoxicity.
Genetically engineered natural killer cells expressing an anti‑CD19 chimeric antigen receptor bind CD19 on B cells and trigger NK cell activation and cytotoxicity (perforin/granzyme), leading to targeted depletion of CD19+ B cells and reduction of pathogenic humoral responses.
YES
DIRECT
Anti-CD19 CAR NK cells bind CD19 on target B cells, triggering NK activation and killing via degranulation (perforin/granzyme) and death-ligand pathways.
An autologous, dual-target CD19/BCMA chimeric antigen receptor T-cell (CAR-T) therapy engineered to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to ablate autoreactive B-cell compartments in refractory SLE.
Autologous T cells engineered with dual CARs targeting CD19 and BCMA bind B cells and plasmablasts/plasma cells, triggering CAR signaling that activates T-cell proliferation and cytolytic activity (perforin/granzyme and cytokines) to deplete CD19+ and BCMA+ compartments, thereby abrogating autoreactive B-cell populations and autoantibody production in refractory SLE.
YES
DIRECT
CD19-binding CAR-T cells engage target cells and, upon activation, induce cytolysis via perforin/granzyme release (and death-receptor/cytokine-mediated apoptosis).
An autologous, dual-target CD19/BCMA chimeric antigen receptor T-cell (CAR-T) therapy engineered to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to ablate autoreactive B-cell compartments in refractory SLE.
Autologous T cells engineered with dual CARs targeting CD19 and BCMA bind B cells and plasmablasts/plasma cells, triggering CAR signaling that activates T-cell proliferation and cytolytic activity (perforin/granzyme and cytokines) to deplete CD19+ and BCMA+ compartments, thereby abrogating autoreactive B-cell populations and autoantibody production in refractory SLE.
YES
DIRECT
BCMA-targeted CAR-T cells bind BCMA+ cells, activate, and kill them via T-cell cytolysis (perforin/granzyme release and cytokine-mediated apoptosis).
Autologous gene-modified T cells engineered to express a second-generation anti-GD2 chimeric antigen receptor (CD3ζ plus co-stimulatory domain), coexpressing interleukin-15 to enhance persistence and expansion, and incorporating an inducible caspase-9 (iC9) safety switch for controlled elimination.
Autologous T cells genetically engineered to express a second-generation anti-GD2 CAR (CD3zeta plus a co-stimulatory domain) that redirects T-cell recognition and cytotoxicity against GD2-positive tumor cells; coexpressed IL-15 enhances T-cell persistence and expansion in vivo; an inducible caspase-9 (iC9) safety switch enables pharmacologic elimination of the cells to control toxicity.
YES
DIRECT
Anti-GD2 CAR T cells recognize GD2 on target cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor pathways).
Autologous gene-modified T cells engineered to express a second-generation anti-GD2 chimeric antigen receptor (CD3ζ plus co-stimulatory domain), coexpressing interleukin-15 to enhance persistence and expansion, and incorporating an inducible caspase-9 (iC9) safety switch for controlled elimination.
Autologous T cells genetically engineered to express a second-generation anti-GD2 CAR (CD3zeta plus a co-stimulatory domain) that redirects T-cell recognition and cytotoxicity against GD2-positive tumor cells; coexpressed IL-15 enhances T-cell persistence and expansion in vivo; an inducible caspase-9 (iC9) safety switch enables pharmacologic elimination of the cells to control toxicity.
NO
INDIRECT
These CAR T cells recognize GD2, not IL‑15Rβ; they kill GD2-positive cells via CAR-activated T-cell cytotoxicity (perforin/granzyme), while IL‑15Rβ-expressing cells are not targeted.