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.
YES
DIRECT
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).
A personalized cancer vaccine composed of patient-specific tumor neoantigens administered subcutaneously to load antigen-presenting cells (primarily dendritic cells), enhance MHC I/II presentation, and expand tumor-specific CD8+ cytotoxic and CD4+ helper T cells to eliminate residual micrometastatic disease and establish immune memory in post-resection stage IIIA lung adenocarcinoma.
Personalized neoantigen peptide vaccine given subcutaneously to be taken up by antigen‑presenting cells (mainly dendritic cells), enhancing MHC I/II presentation and priming/expanding neoantigen‑specific CD8+ cytotoxic and CD4+ helper T cells to eradicate residual tumor cells and establish durable immune memory.
NO
INDIRECT
The vaccine primes neoantigen-specific CD8+ T cells via dendritic cell presentation; these CTLs kill tumor cells presenting neoantigen peptides on MHC I (perforin/granzyme). HLA-DQ–expressing cells are not specifically targeted or killed.
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.
YES
DIRECT
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.
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.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages CD16a on NK cells/macrophages to trigger ADCC/ADCP, killing CD20+ B cells. CD16a-expressing cells serve as effectors and are not themselves killed by the drug.
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.
NO
INDIRECT
CD16b+ cells are not targeted; Obinutuzumab binds CD20 on B cells and engages Fc gamma RIII (CD16) on effector cells to trigger ADCC/ADCP and direct caspase-independent death of CD20+ B cells.