“…B cell hyperactivity is a prominent feature of primary SS, reflected by hypergammaglobulinemia and autoantibody production, among others (2). Consistent with this notion, we showed that B cells from primary SS patients, including antigen-inexperienced naive B cells, express elevated levels of the B cell receptor signaling molecule Bruton's tyrosine kinase (BTK) (3). Elevated BTK levels have been linked to T cell-mediated autoimmune pathology in both rheumatoid arthritis (RA) and primary SS, indicating that there is a proinflammatory feedback loop between B cells and CD41 T cells (3).…”