Autologous T cells are engineered to express a chimeric antigen receptor targeting CD19, enabling MHC-independent recognition and cytotoxic killing of CD19-positive B-lineage cells (naive and memory B cells, plasmablasts). Through T-cell activation and effector mechanisms (perforin/granzyme and cytokines), the therapy depletes B cells, reduces autoantibody production, and helps reset autoreactive B-cell pools in autoimmune disease.