Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse.
Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse.
YES
DIRECT
Allogeneic double-negative T cells (the drug) express NKG2D; binding to ULBP1 (an NKG2D ligand) on target cells triggers MHC-independent cytotoxic degranulation (perforin/granzyme) and cytokine release, leading to target cell lysis/apoptosis.
Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse.
Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse.
YES
DIRECT
RC1012 allogeneic double-negative T cells express NKG2D; binding to ULBP2 (an NKG2D ligand) on target cells triggers MHC-independent cytotoxicity via perforin/granzyme release and IFN-gamma, leading to tumor cell lysis.
Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse.
Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse.
YES
DIRECT
NKG2D on the infused double‑negative T cells binds ULBP3 on target cells, triggering MHC‑independent cytotoxicity via perforin/granzyme release (and IFN‑γ), leading to target cell apoptosis/lysis.
Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse.
Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse.
YES
DIRECT
RC1012 DNT cells express NKG2D and recognize ULBP4 (an NKG2D ligand) on target cells, triggering MHC-independent killing via perforin/granzyme-mediated cytolysis and IFN-γ release.
Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse.
Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse.
YES
DIRECT
DNTs express NKG2D, which binds ULBP5 on target cells, activating cytotoxic granule release (perforin/granzymes) and inflammatory cytokines to lyse the target cell.