Regulatory B cells in skin and connective tissue diseases

While B cells are generally considered to be positive regulators of Immoral immune responses due to their ability to differentiate into plasmablasts/plasma cells and produce antibodies, B cells also modulate immune responses through antigen presentation and cytokine secretion. Moreover, "regulatory B cells" that suppress immune responses have been recognized as an important new component of the immune system. In mice, the function of regulatory B cells is almost exclusively dependent on IL-10. The cell-surface phenotype of murine IL-10-producing regulatory B cells is reported to be CD1d(hi)CD5(+) or CD1d(hi)CD21(hi)CD23IgM(hi), and thus their phenotype overlaps with that of CD5(+) B-la cells, CD1d(hi)CD21(hi)CD23(10)IgM(hi) marginal zone (MZ) B cells, and CD1d(hi)CD21(hi)CD23(hi)IgM(hi) T2-MZ precursor 11 cells. Contrary to earlier work that suggested a minor role for B cells in contact hypersensitivity, regulatory B cells are now known to have a critical inhibitory functions in this type of immune response. Furthermore, studies using murine disease models have demonstrated that regulatory B cells play a significant role in autoimmune connective tissue diseases such as rheumatoid arthritis and systemic lupus erythematosus, as well as organ-specific autoimmune diseases including experimental autoimmune encephalomyelitis and inflammatory bowel disease. In comparison to mouse regulatory 11 cells, little is known regarding their human counterparts. One recent study demonstrates that human CD19(+)CD24(hi)CD38(hi) B cells possess regulatory capacity. Clarifying the molecular mechanisms by which regulatory B cells suppress immune responses will be of great benefit in the development of new B cell-targeted therapeutic strategies. (C) 2010 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.