Patient-derived T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B-cell antigens (e.g., CD19) for MHC-independent recognition and killing of malignant B cells via CD3ζ and costimulatory domains (CD28 or 4-1BB); associated immune activation can lead to CRS and ICANS.
Autologous T cells are genetically engineered to express a chimeric antigen receptor (e.g., anti-CD19) that recognizes B-cell antigens independently of MHC and signals via CD3zeta with CD28 or 4-1BB costimulation, activating cytotoxicity and cytokine release to eliminate malignant B cells (with risks of CRS and ICANS).
CAR-T cells recognize CD19 via the CAR and, upon activation (CD3ζ with costimulation), directly kill CD19+ cells through perforin/granzyme release and death-receptor pathways.
iPSC-derived natural killer cells engineered with dual chimeric antigen receptors targeting CD33 and CLL1 (CLEC12A) to recognize AML blasts and mediate NK cytotoxicity.
iPSC-derived natural killer cells engineered with dual chimeric antigen receptors against CD33 and CLL1 (CLEC12A) bind these antigens on AML blasts, triggering NK-cell activation and targeted cytotoxicity (perforin/granzyme release and cytokine-mediated killing) to eliminate leukemia cells and reduce antigen escape.
CAR-engineered NK cells bind CD33 on target cells, activating NK cytotoxicity and killing via perforin/granzyme-mediated lysis/apoptosis.
iPSC-derived natural killer cells engineered with dual chimeric antigen receptors targeting CD33 and CLL1 (CLEC12A) to recognize AML blasts and mediate NK cytotoxicity.
iPSC-derived natural killer cells engineered with dual chimeric antigen receptors against CD33 and CLL1 (CLEC12A) bind these antigens on AML blasts, triggering NK-cell activation and targeted cytotoxicity (perforin/granzyme release and cytokine-mediated killing) to eliminate leukemia cells and reduce antigen escape.
CAR-NK cells bind CLL1 (CLEC12A) on target cells, triggering NK activation and degranulation (perforin/granzyme) leading to apoptotic/lytic killing, with additional cytokine-mediated cytotoxicity.
iPSC-derived natural killer cells engineered with a chimeric antigen receptor targeting CD33 to direct NK-mediated cytotoxicity against AML cells.
iPSC-derived natural killer cells engineered to express a chimeric antigen receptor that binds CD33 on AML blasts, triggering antigen-specific NK activation and cytotoxicity (perforin/granzyme release and cytokine-mediated killing) to eliminate CD33-positive leukemia cells.
CAR binding to CD33 activates NK-cell cytotoxicity, leading to immune-synapse formation and perforin/granzyme-mediated apoptosis of CD33+ cells (with possible death-receptor/cytokine-mediated killing).
Autologous T cells engineered ex vivo with a chimeric antigen receptor to recognize a B-cell antigen and eliminate pathogenic B cells to suppress humoral autoimmunity in IgA nephropathy and primary membranous nephropathy; administered at 0.5×10^8 or 1×10^8 cells.
Autologous T cells are engineered ex vivo with a chimeric antigen receptor that recognizes a B‑cell antigen. Upon infusion, the CAR-T cells bind and kill B cells, depleting autoreactive/antibody‑producing clones to suppress humoral autoimmunity and reduce pathogenic immune complexes in IgA nephropathy and primary membranous nephropathy.
CAR-T cells recognize CD19 on B cells and directly kill them via T‑cell cytotoxic pathways (perforin/granzyme release and Fas–FasL–mediated apoptosis).