B-lymphocytes govern the pathogenesis of Sjögren's syndrome.

T cells have originally occupied central stage of the debate on the type of lymphocytes governing the pathogenesis of Sjögren's syndrome (SS). However, B cells has since been substituted for T cells, and insights into their functions have revealed that they accomplish various tasks. Beyond the paradigm that T lymphocytes maintain strict control over B lymphocytes, these latter cells solicit their own help from the former, release a flurry of cytokines, and act as antigen- presenting cells. In SS, excessive of the B cell-activating factor (BAFF) may cause B-cell quantitative anomalies, such as inflation of mature B (Bm)2/Bm2' cells in the circulation, or accumulation of transitional type 2, marginal zone (MZ) and memory B cells within the exocrine gland infiltrates. These excesses are also associated with B-cell qualitative anomalies, such as the internal synthesis of BAFF, and a default mechanism that promotes the autoantibody production in ectopic germinal centers or MZ equivalents. Thus, SS should rather be conceived as a quintessential model for B cell-induced autoimmunity. Such a view opens novel prospects for treatment, and indeed B cell-ablative therapy has already been shown to be beneficial to these patients.