Journal
IMMUNOLOGICAL REVIEWS
Volume 233, Issue -, Pages 146-161Publisher
WILEY
DOI: 10.1111/j.0105-2896.2009.00855.x
Keywords
B cells; autoimmunity; Toll-like receptor; interleukin-10; immunoregulation; feedforward loop
Categories
Funding
- Hertie Stiftung
- Deutsche Forschungsgemeninschaft
- Medical Research Council [G9900991B, G0801924] Funding Source: researchfish
- MRC [G0801924] Funding Source: UKRI
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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.
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