Off-the-shelf, gene-modified T cells expressing dual chimeric antigen receptors targeting CD19 and BCMA to deplete B cells, plasmablasts, and plasma cells in autoimmune hemolytic anemia.
Allogeneic, off-the-shelf T cells engineered with dual chimeric antigen receptors targeting CD19 and BCMA. Binding to CD19+ B cells and BCMA+ plasmablasts/plasma cells activates the CAR T cells to kill these cells, depleting autoreactive antibody-producing compartments and reducing pathogenic autoantibodies in autoimmune hemolytic anemia.
Anti-CD19 CAR T cells bind CD19 on target B cells, form an immune synapse, and directly kill them via perforin/granzyme-mediated cytolysis and death receptor pathways (e.g., Fas-FasL).
Off-the-shelf, gene-modified T cells expressing dual chimeric antigen receptors targeting CD19 and BCMA to deplete B cells, plasmablasts, and plasma cells in autoimmune hemolytic anemia.
Allogeneic, off-the-shelf T cells engineered with dual chimeric antigen receptors targeting CD19 and BCMA. Binding to CD19+ B cells and BCMA+ plasmablasts/plasma cells activates the CAR T cells to kill these cells, depleting autoreactive antibody-producing compartments and reducing pathogenic autoantibodies in autoimmune hemolytic anemia.
BCMA engagement activates the dual CAR T cells to form an immune synapse and kill BCMA+ cells via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Autologous gene-modified T cells engineered to express a CAR targeting CD70, eliminating CD70-positive activated B and T lymphocytes (and some APCs) to suppress CD70–CD27–mediated immune activation in MDR-SRNS.
Autologous T cells are engineered to express a chimeric antigen receptor that binds CD70 on activated B and T lymphocytes (and some APCs). Antigen engagement triggers CAR signaling, leading to T-cell activation and cytotoxic killing (perforin/granzyme and cytokine-mediated) of CD70+ cells, thereby disrupting CD70–CD27 co-stimulation and suppressing pathogenic immune activation in MDR-SRNS.
CAR-T cells bind CD70 on target cells and, upon CAR signaling, kill CD70+ cells via perforin/granzyme-mediated cytolysis (and cytokine/death-receptor pathways).
Adoptive cell therapy consisting of a single IV infusion of ex vivo expanded autologous tumor-reactive T cells to augment anti-tumor immunity.
Autologous T cells are isolated and expanded ex vivo based on functional reactivity to tumor antigens. After infusion, these TCR-mediated tumor‑specific CD4+/CD8+ T cells recognize peptide–MHC complexes on tumor cells, release cytotoxic granules and inflammatory cytokines, and augment anti‑tumor immunity.
Adoptively transferred tumor‑reactive T cells recognize the neoantigen peptide–HLA-I complex via their TCR and directly kill target cells through perforin/granzyme release (and Fas–FasL–mediated apoptosis).
Adoptive cell therapy consisting of a single IV infusion of ex vivo expanded autologous tumor-reactive T cells to augment anti-tumor immunity.
Autologous T cells are isolated and expanded ex vivo based on functional reactivity to tumor antigens. After infusion, these TCR-mediated tumor‑specific CD4+/CD8+ T cells recognize peptide–MHC complexes on tumor cells, release cytotoxic granules and inflammatory cytokines, and augment anti‑tumor immunity.
Adoptively transferred tumor‑reactive T cells recognize the peptide–HLA-I complex via their TCR and kill target cells via perforin/granzyme release and Fas–FasL–mediated apoptosis, with cytokines augmenting cytotoxicity.