Autologous gene-modified T lymphocytes engineered to express a chimeric antigen receptor that recognizes CD19 and targets within the BAFF (BLyS) axis (e.g., BAFF-R/TACI/BCMA), enabling activation and cytolytic depletion of pathogenic B cells/plasmablasts to reduce BCR signaling, germinal center activity, and autoantibody production in refractory autoimmune disease.
Autologous T cells engineered with a chimeric antigen receptor that recognizes CD19 and BAFF-axis receptors (BAFF-R/TACI/BCMA), leading to antigen-dependent activation and cytolytic elimination of B cells and plasmablasts. This depletes pathogenic B-lineage cells, disrupts BAFF-mediated survival signals, and reduces BCR signaling, germinal center activity, and autoantibody production in autoimmune disease.
CAR T cells recognize CD19 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous gene-modified T lymphocytes engineered to express a chimeric antigen receptor that recognizes CD19 and targets within the BAFF (BLyS) axis (e.g., BAFF-R/TACI/BCMA), enabling activation and cytolytic depletion of pathogenic B cells/plasmablasts to reduce BCR signaling, germinal center activity, and autoantibody production in refractory autoimmune disease.
Autologous T cells engineered with a chimeric antigen receptor that recognizes CD19 and BAFF-axis receptors (BAFF-R/TACI/BCMA), leading to antigen-dependent activation and cytolytic elimination of B cells and plasmablasts. This depletes pathogenic B-lineage cells, disrupts BAFF-mediated survival signals, and reduces BCR signaling, germinal center activity, and autoantibody production in autoimmune disease.
CAR T cells recognize BAFF-R via the CAR, become activated, and directly kill BAFF-R–expressing cells through perforin/granzyme-mediated cytolysis (and Fas–FasL pathways).
Autologous gene-modified T lymphocytes engineered to express a chimeric antigen receptor that recognizes CD19 and targets within the BAFF (BLyS) axis (e.g., BAFF-R/TACI/BCMA), enabling activation and cytolytic depletion of pathogenic B cells/plasmablasts to reduce BCR signaling, germinal center activity, and autoantibody production in refractory autoimmune disease.
Autologous T cells engineered with a chimeric antigen receptor that recognizes CD19 and BAFF-axis receptors (BAFF-R/TACI/BCMA), leading to antigen-dependent activation and cytolytic elimination of B cells and plasmablasts. This depletes pathogenic B-lineage cells, disrupts BAFF-mediated survival signals, and reduces BCR signaling, germinal center activity, and autoantibody production in autoimmune disease.
CAR T cells recognize TACI via the CAR, triggering antigen-dependent T‑cell activation and killing of TACI+ cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous gene-modified T lymphocytes engineered to express a chimeric antigen receptor that recognizes CD19 and targets within the BAFF (BLyS) axis (e.g., BAFF-R/TACI/BCMA), enabling activation and cytolytic depletion of pathogenic B cells/plasmablasts to reduce BCR signaling, germinal center activity, and autoantibody production in refractory autoimmune disease.
Autologous T cells engineered with a chimeric antigen receptor that recognizes CD19 and BAFF-axis receptors (BAFF-R/TACI/BCMA), leading to antigen-dependent activation and cytolytic elimination of B cells and plasmablasts. This depletes pathogenic B-lineage cells, disrupts BAFF-mediated survival signals, and reduces BCR signaling, germinal center activity, and autoantibody production in autoimmune disease.
CAR T cells recognize BCMA on target cells, form an immune synapse, and kill via T‑cell cytotoxic mechanisms (perforin/granzyme release and death‑receptor signaling).
A humanized IgG1 monoclonal antibody administered subcutaneously that binds ILT7 on plasmacytoid dendritic cells, leading to Fc-mediated depletion/inhibition of pDCs and reduced type I interferon (IFN-α/β) signaling.
Humanized IgG1 monoclonal antibody that binds ILT7 on plasmacytoid dendritic cells and, via Fc effector functions, depletes/inhibits pDCs, reducing type I interferon (IFN-α/β) signaling and downstream inflammation.
The IgG1 antibody binds ILT7 on pDCs and engages Fc effector functions (ADCC/ADCP ± complement) to deplete ILT7+ cells.