Autologous, gene-modified bispecific CD19/CD20-directed CAR T-cell therapy designed to deplete B-lineage cells to suppress B-cell–driven autoimmunity in refractory SLE and lupus nephritis.
Autologous T cells are gene-modified to express a bispecific CAR targeting CD19 and CD20 on B-lineage cells; engagement activates the CAR T cells to kill and deplete B cells and plasmablasts, reducing autoantibody production and B cell–driven autoimmunity in SLE and lupus nephritis.
CAR T cells bind CD19 on B-lineage cells via the bispecific CD19/CD20 CAR, triggering T-cell activation and immune-synapse formation, leading to perforin/granzyme-mediated cytolysis and apoptosis of CD19+ cells.
Autologous, gene-modified bispecific CD19/CD20-directed CAR T-cell therapy designed to deplete B-lineage cells to suppress B-cell–driven autoimmunity in refractory SLE and lupus nephritis.
Autologous T cells are gene-modified to express a bispecific CAR targeting CD19 and CD20 on B-lineage cells; engagement activates the CAR T cells to kill and deplete B cells and plasmablasts, reducing autoantibody production and B cell–driven autoimmunity in SLE and lupus nephritis.
Bispecific CD19/CD20 CAR T cells bind CD20 on B-lineage cells, become activated, and directly lyse the target cells via perforin/granzyme-mediated cytotoxicity (and Fas/FasL signaling).
Intravenous type II, glycoengineered humanized anti-CD20 monoclonal antibody that binds CD20 on B cells, inducing direct cell death and strong Fc-mediated ADCC/ADCP, leading to B-cell depletion.
Type II, glycoengineered humanized IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc gamma RIIIa engagement leading to strong ADCC/ADCP and by inducing direct, caspase-independent cell death.
Binds CD20 on B cells, inducing direct caspase-independent cell death and recruiting FcγRIIIa-expressing effector cells (e.g., NK cells, macrophages) to mediate ADCC/ADCP, leading to B-cell killing.
Autologous T cells genetically modified to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on plasmablasts/plasma cells to eliminate antibody-secreting cells and modulate autoimmunity.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes BCMA (TNFRSF17) on plasmablasts and plasma cells. Upon antigen binding, CAR signaling activates the T cells to kill BCMA+ cells via cytotoxic effector functions and cytokine release, depleting antibody-secreting cells and reducing pathogenic autoantibodies to modulate autoimmunity.
CAR recognition of BCMA activates the engineered T cells to kill BCMA+ cells via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with supportive cytokine effects.
Autologous CAR T cells targeting CD19 on B-lineage cells (naive, memory, some plasmablasts) to deplete autoreactive B cells and reduce antigen presentation and autoantibody production.
Autologous T cells are genetically modified to express a chimeric antigen receptor targeting CD19; upon binding CD19 on B-lineage cells (naive, memory, some plasmablasts), CAR signaling activates cytotoxic pathways (perforin/granzyme, death receptors) to deplete B cells, thereby reducing antigen presentation and autoantibody production and helping reset dysregulated humoral immunity.
CD19 CAR T cells bind CD19 on B-lineage cells; CAR signaling triggers perforin/granzyme release and death-receptor pathways (e.g., Fas/FasL), causing apoptosis/lysis of the target cells.