Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19, leading to cytotoxic depletion of CD19+ B-lineage cells and a B-cell reset in SLE.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CD19. Upon binding CD19 on B-lineage cells, the CAR T cells become activated and mediate cytotoxic killing of CD19+ B cells and plasmablasts, leading to B-cell depletion and subsequent immune reset with reduced autoantibody production and inflammatory signaling.
CD19-targeted CAR T cells bind CD19 on B-lineage cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
CRISPR-edited, allogeneic, second-generation anti-CD19 CAR-T (FMC63 scFv; CD28 costimulatory and CD3ζ signaling domains) with TRAC knockout to remove endogenous TCR and SPPL3 (Power3) knockout to alter glycosylation (“glycan shielding”), aiming to reduce GVHD, lessen alloimmune recognition, and improve persistence against CD19+ malignant B cells.
CRISPR-edited, allogeneic second-generation anti-CD19 CAR-T cells (FMC63 scFv with CD28 costimulation and CD3ζ signaling) mediate CAR-driven activation and cytotoxic killing of CD19+ B cells. TRAC knockout removes the endogenous TCR to reduce graft-versus-host disease, while SPPL3 (Power3) knockout alters glycosylation to lessen alloimmune recognition and enhance persistence/expansion.
Anti-CD19 CAR-T cells bind CD19 on target B cells, triggering CD28/CD3ζ signaling and formation of an immunologic synapse that mediates perforin/granzyme release (and death-receptor signaling), inducing apoptosis of CD19+ cells.
Humanized IgG monoclonal antibody (JSP191) administered subcutaneously that targets CD117 (c‑Kit), blocking SCF–c‑Kit signaling to deplete/inhibit KIT+ cells, especially tissue mast cells, thereby reducing mediator release in chronic urticaria.
Humanized IgG monoclonal antibody targeting CD117 (c‑Kit) that blocks stem cell factor (SCF) binding/signaling, leading to depletion or inhibition of KIT+ cells—particularly mast cells and hematopoietic stem/progenitor cells—thereby reducing mast-cell survival/activation and mediator release.
Binds CD117 and blocks SCF–c‑Kit survival signaling, leading to apoptosis/depletion of KIT+ cells (with potential contribution from Fc-mediated effector functions).
Autologous CD7-directed chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are engineered to express a CD7-targeted CAR (CD3ζ with costimulation); upon CD7 engagement, CAR signaling activates and expands T cells to kill CD7+ malignant cells via perforin/granzyme and cytokine-mediated cytotoxicity in r/r T-ALL, lymphoblastic lymphoma, and CD7-positive AML.
Autologous T cells are genetically engineered to express a CD7-directed chimeric antigen receptor (with CD3ζ signaling and costimulatory domains). Upon binding CD7 on malignant cells, CAR activation drives T‑cell activation, expansion, and cytotoxic killing via perforin/granzyme release and cytokine-mediated mechanisms, depleting CD7+ leukemic/lymphoma cells.
CD7-targeted CAR T cells bind CD7 on target cells and kill them via CAR-activated cytotoxicity, primarily perforin/granzyme-mediated lysis (with cytokine/Fas–FasL contributions).
Donor-derived, ex vivo–expanded polyclonal CD8+ and CD4+ T cells specific for Epstein–Barr virus antigens (e.g., EBNA, LMP) administered post-transplant as adoptive cellular immunotherapy to restore antiviral immunity and eliminate EBV-infected/malignant cells.
Donor-derived, ex vivo–expanded EBV-specific CD8+/CD4+ T cells use their native, HLA-restricted TCRs to recognize EBV antigens (e.g., EBNA, LMP) on infected or malignant cells and eliminate them via perforin/granzyme cytotoxicity and Th1 cytokines, restoring antiviral immunity and controlling EBV-driven lymphoproliferation with low GVHD risk.
EBV-specific T cells recognize EBNA1-derived peptides presented by HLA on target cells via their native TCRs and kill them through perforin/granzyme (and Fas/FasL)–mediated apoptosis.