Engineered universal T-cell therapy expressing a chimeric NK receptor that enables NK-like recognition of stress-induced NK ligands on dysregulated/activated immune cells. Engagement triggers T-cell activation, perforin/granzyme-mediated cytotoxicity, and immunomodulation to eliminate pathogenic immune cells driving steroid-refractory/resistant or steroid-dependent GVHD. Administered IV in Phase 1 SAD/MAD dosing.
Engineered universal T cells expressing a chimeric NK receptor (NK-like CAR, e.g., NKG2D-based) that recognizes stress-induced NK ligands on activated/dysregulated immune cells; receptor engagement triggers T-cell activation with perforin/granzyme-mediated cytotoxicity and immunomodulation to eliminate pathogenic alloreactive T cells and antigen-presenting cells driving steroid-refractory/resistant GVHD.
Engineered T cells express an NKG2D-based chimeric receptor that binds MICB on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (apoptosis).
Adoptive T-cell therapy from healthy CMV-seropositive donors; HLA-matched CMV-specific T cells recognize CMV antigens on glioblastoma cells and kill them via T-cell cytotoxicity and cytokine release.
Allogeneic CMV-specific T cells expanded from seropositive donors and HLA-matched to the patient recognize CMV peptide–HLA complexes on glioblastoma cells via their native TCRs, leading to targeted cytotoxicity (perforin/granzyme) and cytokine-mediated antitumor activity.
CMV-specific T cells recognize CMV peptide–HLA class I via their native TCR and kill target cells through cytotoxic T-lymphocyte mechanisms (perforin/granzyme-mediated apoptosis, potentially Fas–FasL), with supportive cytokine effects.
Engineered universal T-cell therapy expressing a chimeric NK receptor that enables NK-like recognition of stress-induced NK ligands on dysregulated/activated immune cells. Engagement triggers T-cell activation, perforin/granzyme-mediated cytotoxicity, and immunomodulation to eliminate pathogenic immune cells driving steroid-refractory/resistant or steroid-dependent GVHD. Administered IV in Phase 1 SAD/MAD dosing.
Engineered universal T cells expressing a chimeric NK receptor (NK-like CAR, e.g., NKG2D-based) that recognizes stress-induced NK ligands on activated/dysregulated immune cells; receptor engagement triggers T-cell activation with perforin/granzyme-mediated cytotoxicity and immunomodulation to eliminate pathogenic alloreactive T cells and antigen-presenting cells driving steroid-refractory/resistant GVHD.
Engineered T cells express an NKG2D-based chimeric receptor that binds ULBP1 on target cells, triggering activation and perforin/granzyme-mediated cytotoxic killing.
Engineered universal T-cell therapy expressing a chimeric NK receptor that enables NK-like recognition of stress-induced NK ligands on dysregulated/activated immune cells. Engagement triggers T-cell activation, perforin/granzyme-mediated cytotoxicity, and immunomodulation to eliminate pathogenic immune cells driving steroid-refractory/resistant or steroid-dependent GVHD. Administered IV in Phase 1 SAD/MAD dosing.
Engineered universal T cells expressing a chimeric NK receptor (NK-like CAR, e.g., NKG2D-based) that recognizes stress-induced NK ligands on activated/dysregulated immune cells; receptor engagement triggers T-cell activation with perforin/granzyme-mediated cytotoxicity and immunomodulation to eliminate pathogenic alloreactive T cells and antigen-presenting cells driving steroid-refractory/resistant GVHD.
Engineered T cells bearing an NKG2D-based chimeric receptor bind ULBP2 on target cells, triggering T-cell activation and perforin/granzyme-mediated lysis of the target cells.
Engineered universal T-cell therapy expressing a chimeric NK receptor that enables NK-like recognition of stress-induced NK ligands on dysregulated/activated immune cells. Engagement triggers T-cell activation, perforin/granzyme-mediated cytotoxicity, and immunomodulation to eliminate pathogenic immune cells driving steroid-refractory/resistant or steroid-dependent GVHD. Administered IV in Phase 1 SAD/MAD dosing.
Engineered universal T cells expressing a chimeric NK receptor (NK-like CAR, e.g., NKG2D-based) that recognizes stress-induced NK ligands on activated/dysregulated immune cells; receptor engagement triggers T-cell activation with perforin/granzyme-mediated cytotoxicity and immunomodulation to eliminate pathogenic alloreactive T cells and antigen-presenting cells driving steroid-refractory/resistant GVHD.
Engineered T cells expressing an NKG2D-based chimeric receptor bind ULBP3 on target cells, triggering T-cell activation and immune synapse formation that leads to perforin/granzyme-mediated lysis (and possibly Fas/FasL apoptosis).