Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
YES
DIRECT
ULBP6 is an NKG2D ligand. Vγ9Vδ2 T cells express NKG2D; engagement of NKG2D by ULBP6 on target cells activates these T cells to kill via perforin/granzyme (and death receptor) pathways.
Bispecific T-cell engager (BiTE) antibody that links CD19 on B cells to CD3 on T cells to activate cytotoxic T-cell killing of malignant B cells.
A CD19xCD3 bispecific (BiTE) antibody that binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T-cell cytotoxicity and lyse CD19-positive malignant B cells.
YES
DIRECT
Blinatumomab bridges CD19 on target cells to CD3 on T cells, forming an immunological synapse and triggering T‑cell–mediated killing (perforin/granzyme and Fas–FasL apoptosis) of CD19+ cells.
Bispecific T-cell engager (BiTE) antibody that links CD19 on B cells to CD3 on T cells to activate cytotoxic T-cell killing of malignant B cells.
A CD19xCD3 bispecific (BiTE) antibody that binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T-cell cytotoxicity and lyse CD19-positive malignant B cells.
NO
INDIRECT
Blinatumomab binds CD3 on T cells to activate and redirect them to CD19+ cells; the T cells then kill CD19-expressing B cells via perforin/granzyme-mediated cytotoxicity. CD3+ cells are not targeted for killing.
Anti-CD22 antibody–drug conjugate that delivers calicheamicin intracellularly, causing DNA double-strand breaks and cytotoxicity after internalization.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; after binding CD22 on B cells and internalization, the payload is released to bind the DNA minor groove, causing double-strand breaks and apoptosis.
YES
DIRECT
The anti-CD22 ADC binds CD22, is internalized, and releases calicheamicin, which binds the DNA minor groove causing double-strand breaks and apoptosis in target cells.
Anti-CD22 antibody–drug conjugate that delivers calicheamicin intracellularly, causing DNA double-strand breaks and cytotoxicity after internalization.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; after binding CD22 on B cells and internalization, the payload is released to bind the DNA minor groove, causing double-strand breaks and apoptosis.
NO
INDIRECT
Inotuzumab ozogamicin targets CD22 on B cells, is internalized, and releases calicheamicin, which binds the DNA minor groove to cause double-strand breaks and apoptosis.