IL-10-producing regulatory B cells and plasmocytes: Molecular mechanisms and disease relevance. (August 2019)

• Record Type: Journal Article
• Authors: Cerqueira, Catia; Manfroi, Benoît; Fillatreau, Simon
• Is Part Of: Seminars in immunology. Volume 44(2019)
• Publication Date: 2019-08
• Subjects: B cell -- Plasma cell -- Cytokine -- IL-10 -- Autoimmune disease; Immunology -- Periodicals; Allergy and Immunology -- Periodicals; Immunity -- Periodicals; Immunologie -- Périodiques; Electronic journals; 616.079
• DOI: 10.1016/j.smim.2019.101323
• Languages: English
• ISSNs: 1044-5323

Abstract

Highlights: IL-10 is regulated at epigenetic, transcriptional and post-transcriptional levels. IL-10 expression in TLR-activated B cells involves the BCR signaling pathway. Plasmocytes and memory B cells can express IL-10 in human autoimmune diseases. Abstract: It has long been assumed that the functions of B cells reflected the roles of antibodies. However, B cells also decisively influence immunity via antibody-independent mechanisms including the presentation of antigen to T cells and the secretion of cytokines. In fact, B cell depletion therapy improves the course of autoimmune diseases such as multiple sclerosis by removing pro-inflammatory cytokine-producing B cells rather than by reducing autoantibody levels. Remarkably, B cells can also produce anti-inflammatory cytokines, and subsequently suppress immunity, providing protection from autoimmune diseases while interfering with beneficial responses against pathogens and cancers. A major mediator of this B cell regulatory function is their secretion of IL-10. There is considerable interest in identifying the mechanisms inducing the expression of IL-10 in B cells during the course of their activation. Here, we review the molecular mechanisms controlling IL-10 expression in B cells, and the evidence that IL-10-producing B cells play a protective role in human autoimmune diseases, underlying the relevance of this immunosuppressive axis for therapy.