Autologous, genetically engineered T cells expressing a chimeric antigen receptor targeting CD19 to deplete CD19+ B-lineage cells (B cells and plasmablasts) and reduce pathogenic anti–acetylcholine receptor autoantibodies in refractory AChR-positive myasthenia gravis.
Autologous T cells engineered to express an anti‑CD19 chimeric antigen receptor bind and kill CD19+ B cells/plasmablasts via CAR‑triggered cytotoxicity, depleting B‑lineage cells and reducing pathogenic anti‑AChR autoantibodies in myasthenia gravis.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on B-lineage cells and kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis; also Fas-FasL).
Autologous, fully human anti-CD19 CAR T-cell therapy given as a single IV dose (~1×10^8 CAR+ T cells) to eliminate CD19+ B cells/plasmablasts via T-cell cytotoxicity, inducing deep B-cell depletion and an immune reset to reduce pathogenic autoantibodies.
Autologous T cells engineered to express a fully human anti-CD19 CAR (CD8alpha hinge/transmembrane, CD28 costimulatory, CD3-zeta signaling). After infusion, they bind CD19 on B cells and plasmablasts, activate and mediate cytotoxic killing, producing deep B-cell depletion and an immune reset that lowers pathogenic autoantibodies.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B cells, activate via CD28/CD3ζ signaling, and kill target cells through T-cell cytotoxic pathways (perforin/granzyme-mediated apoptosis, and related mechanisms).
Gene-modified natural killer T cells engineered to express a chimeric antigen receptor targeting CD70; infused after lymphodepleting chemotherapy to treat CD70-positive advanced solid tumors via largely MHC-independent cytotoxicity and cytokine release.
Autologous natural killer T cells engineered to express a CD70-specific chimeric antigen receptor bind CD70 on tumor cells and, upon CAR activation, execute largely MHC-independent killing via perforin/granzyme release and pro-inflammatory cytokine secretion; lymphodepleting cyclophosphamide/fludarabine is used to enhance engraftment and expansion.
YES
DIRECT
CAR-NKT cells recognize CD70 and kill target cells via MHC-independent perforin/granzyme-mediated cytolysis, with supportive pro-inflammatory cytokine effects.
Anti-CD22 antibody-drug conjugate that delivers calicheamicin to CD22-positive blasts, causing DNA double-strand breaks and apoptosis.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; upon binding CD22 on B-cell blasts, the ADC is internalized and releases calicheamicin that binds the DNA minor groove, causing double-strand breaks and apoptosis.
YES
DIRECT
The anti-CD22 ADC binds CD22, is internalized, and releases calicheamicin intracellularly, causing DNA double-strand breaks and apoptosis of CD22-positive cells.
Monoclonal antibodies targeting CD20 on B cells; deplete malignant B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptosis.
Unconjugated anti‑CD20 IgG antibodies bind CD20 on B cells and mediate cell depletion primarily via Fc‑dependent antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and by triggering direct apoptosis of CD20+ malignant (and normal) B cells.
YES
DIRECT
Anti-CD20 IgG binds CD20 on B cells and eliminates them via Fc-mediated ADCC (e.g., NK cells), complement-dependent cytotoxicity (CDC), and by triggering direct apoptosis of CD20+ cells.