Suppressive functions of activated B cells in autoimmune diseases reveal the dual roles of Toll-like receptors in immunity

Vicky Lampropoulou, Elisabeth Calderon-Gomez, Toralf Roch, Patricia Neves, Ping Shen, Ulrik Stervbo, Pierre Boudinot, Stephen M. Anderton, Simon Fillatreau

Research output: Contribution to journalLiterature reviewpeer-review


B lymphocytes contribute to immunity through production of antibodies, antigen presentation to T cells, and secretion of cytokines. B cells are generally considered in autoimmune diseases as drivers of pathogenesis. This view is certainly justified, given the successful utilization of the B cell-depleting reagent rituximab in patients with rheumatoid arthritis or other autoimmune pathologies. In a number of cases, however, the depletion of B cells led to an exacerbation of symptoms in patients with autoimmune disorders. In a similar manner, mice lacking B cells can develop an aggravated course of disease in several autoimmune models. These paradoxical observations are now explained by the concept that activated B cells can suppress immune responses through the production of cytokines, especially interleukin-10. Here, we review the stimulatory signals that induce interleukin-10 secretion and suppressive functions in B cells and the phenotype of the B cells with such characteristics. Finally, we formulate a model explaining how this process of immune regulation by activated B cells can confer advantageous properties to the immune system in its combat with pathogens. Altogether, this review proposes that B-cell-mediated regulation is a fundamental property of the immune system, with features of great interest for the development of new cell-based therapies for autoimmune diseases.

Original languageEnglish
Pages (from-to)146-161
Number of pages16
JournalImmunological reviews
Publication statusPublished - Jan 2010


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