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 cellinduced
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.
Keywords: B lymphocyte, Sjogren's syndrome, B cell activating factor, ectopic germinal centers, T cells, pathogenesis, lymphocytes, cytokines, antigen-presenting cells, marginal zone, internal synthesis, MZ equivalents, B cell-ablative therapy, salyvary gland (SG), rheumatoid arthritis (RA).
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