Donor-derived, partially HLA-matched virus-specific T lymphocytes enriched for IFN-γ–secreting CD8+/CD4+ T cells reactive to adenovirus, CMV, and EBV antigens; manufactured using CliniMACS cytokine capture and infused to restore antiviral immunity by HLA-restricted recognition and cytotoxic killing of infected cells.
Adoptive transfer of donor-derived, partially HLA-matched virus-specific CD8+/CD4+ T cells selected for IFN-γ secretion. These unengineered T cells use native TCRs to recognize HLA-presented adenovirus/CMV/EBV peptides on infected cells, secrete Th1 cytokines, and kill targets via perforin/granzyme, restoring antiviral immunity.
Virus-specific T cells recognize HLA-presented adenoviral peptides via their native TCRs and directly kill the infected cells by perforin/granzyme-mediated apoptosis (and related cytotoxic pathways).
Donor-derived, partially HLA-matched virus-specific T lymphocytes enriched for IFN-γ–secreting CD8+/CD4+ T cells reactive to adenovirus, CMV, and EBV antigens; manufactured using CliniMACS cytokine capture and infused to restore antiviral immunity by HLA-restricted recognition and cytotoxic killing of infected cells.
Adoptive transfer of donor-derived, partially HLA-matched virus-specific CD8+/CD4+ T cells selected for IFN-γ secretion. These unengineered T cells use native TCRs to recognize HLA-presented adenovirus/CMV/EBV peptides on infected cells, secrete Th1 cytokines, and kill targets via perforin/granzyme, restoring antiviral immunity.
Virus-specific T cells recognize CMV peptide–HLA complexes via native TCRs and kill infected cells by CTL degranulation (perforin/granzyme), with possible Fas–FasL engagement.
Donor-derived, partially HLA-matched virus-specific T lymphocytes enriched for IFN-γ–secreting CD8+/CD4+ T cells reactive to adenovirus, CMV, and EBV antigens; manufactured using CliniMACS cytokine capture and infused to restore antiviral immunity by HLA-restricted recognition and cytotoxic killing of infected cells.
Adoptive transfer of donor-derived, partially HLA-matched virus-specific CD8+/CD4+ T cells selected for IFN-γ secretion. These unengineered T cells use native TCRs to recognize HLA-presented adenovirus/CMV/EBV peptides on infected cells, secrete Th1 cytokines, and kill targets via perforin/granzyme, restoring antiviral immunity.
Virus-specific T cells recognize HLA-presented EBV peptides via native TCRs and kill target cells through CTL cytotoxicity (perforin/granzyme; Fas–FasL).
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
rATG contains polyclonal IgG that binds CD4 on T cells, triggering complement-dependent lysis and Fc-mediated ADCC/phagocytosis (and apoptosis), resulting in direct depletion of CD4+ cells.
Gene-modified, off-the-shelf allogeneic NK-92 cell therapy expressing an NKG2D chimeric antigen receptor that binds stress-induced ligands (e.g., MICA/MICB) on tumor cells to trigger NK-cell cytotoxicity (perforin/granzyme release and cytokine secretion).
Allogeneic NK-92 cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced NKG2D ligands (e.g., MICA/MICB/ULBPs) on tumor cells, triggering NK-cell activation and CAR signaling to drive perforin/granzyme-mediated cytotoxicity and cytokine secretion, resulting in tumor cell lysis.
NKG2D-CAR NK-92 cells bind MICA on target cells, triggering NK activation and immune synapse formation, leading to perforin/granzyme-mediated lysis of the MICA-expressing cells.