Patient-specific cancer vaccine delivering tumor neoantigens to antigen-presenting cells to prime and expand tumor-specific CD8+ and CD4+ T cells.
Patient-specific neoantigen peptides are delivered to antigen-presenting cells for MHC I/II presentation, priming and expanding tumor-specific CD8+ and CD4+ T cells to generate targeted antitumor immunity.
YES
INDIRECT
The vaccine delivers neoantigen peptides to APCs, priming CD4+ and CD8+ T cells. These T cells then recognize the neoantigen–MHC complexes on tumor cells and kill them via perforin/granzyme or Fas–FasL pathways.
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, which binds ULBP6 on target cells, triggering MHC-independent cytotoxicity via perforin/granzyme release (with IFN-γ) to lyse the target cells.
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 express DNAM‑1 (CD226) that binds CD155 (PVR) on target cells, triggering MHC‑independent cytotoxic degranulation (perforin/granzyme) and IFN‑γ release to kill the cells.
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 express DNAM‑1 (CD226) and bind CD112 (NECTIN2) on target cells, triggering MHC‑independent cytotoxic degranulation (perforin/granzymes) and IFN‑γ release, leading to target cell lysis/apoptosis.
A chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibodies (e.g., anti-PLA2R/THSD7A) and downstream complement-mediated podocyte injury in idiopathic membranous nephropathy.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing pathogenic autoantibodies and downstream complement-mediated tissue injury.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (MAC-mediated lysis) and FcγR-mediated ADCC by NK cells/macrophages; it can also trigger apoptosis.