Are the B cells cast with the leading part in the S jogren's syndrome scenario?

The autoimmune exocrinopathy S jögren's syndrome ( SS ) is characterized by mononuclear cell (MNC) infiltrates of exocrine glands and overactivity of B lymphocytes. Although T cells have long been perceived as the prime effectors, increasing evidence indicates that the key role is rather served by B cells. Among related abnormalities are rheumatoid factor (RF), anti‐ SSA / R o, and anti‐ SSB / L a antibodies ( A b). Also, supporting this view is our finding of an increase in the number of circulating naïve mature B ( B m) cells, with a reciprocal decrease in that of memory B cells. Furthermore, a ratio of B m2‐plus‐ B m2′ cells to early B m5‐plus‐late B m5 above 5 is diagnostic. This variation partly reflects the migration of active memory B cells into the exocrine glands of the patients, as well as into their skin. More recently, the B ‐cell‐activating factor of the TNF family ( BAFF ) has been endorsed with a pivotal role in B ‐cell survival and hence implicated in the pathogenesis of autoimmunity. In practice, B cells have turned quite attractive as a target for biotherapy. For example, treatment with anti‐ CD 20 A b has afforded some benefits in this disease, while BAFF blockers are still on the way, but should expand our armamentarium for treating SS . With such B ‐cell‐directed biotherapies in mind, we delineate herein the distinguishing traits of B lymphocytes in SS .