In affected tissues of autoimmune patients, lymphoid follicles with germinal centers (GCs) - the so-called tertiary lymphoid structures - frequently form. This clearly indicates B-cell activation and differentiation into plasma cells and memory B cells. These aggregates - T cells surrounding CD20 + B cells - form GC-like structures in patients with RA or other autoimmune diseases. Moreover, Seisuke Takemura of the Mayo Clinic and colleagues demonstrated in mice that T-cell activation in RA is B-cell dependent. 2 Treatment with B cell-depleting antibodies destroyed the extrafollicular GCs, removed dendritic follicular cell networks, and disrupted T-cell activation.
In autoimmunity, B cells participate in various processes. 3 For instance, B cells produce proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and IL-6. On the other hand, B cells produce IL-10, which inhibits inflammation.
B cells also make autoantibodies that can trigger autoimmunity. Patients with RA, for example, often exhibit autoantibodies ...
