title: Regulatory B cells play a key role in immune system balance.
abstract: Regulatory B cells (Bregs) may act earlier than regulatory T cells (Tregs) and may play as important a role in autoimmune and allergic diseases. Obstacles to the investigation of Bregs are the same as those encountered for Tregs: the regulatory effects are short-lived in some cases, there is no consistent phenotype (C5 expression is neither indispensable nor sufficient), differences exist across species (e.g., between humans and mice), and there are a number of suppression modalities (IL-10, TGF-beta, expression of proapoptotic membrane molecules) that vary across Breg subtypes. The Breg subtypes may be homologous to the Treg subtypes (Br1 cells expressing IL-10, Br3 cells expressing TGF-beta, and B-Foxp3 cells), although the Br1 subtype seems to predominate. Nevertheless, differences with Treg cells may exist: Breg activation may chiefly involve the toll-like receptors rather than the antigen receptor; and Bregs act earlier, facilitating the recruitment of Tregs then disappearing once the Tregs become operational. Bregs make a major contribution to autoimmune disorders associated with several forms of immune deficiency, as well as to the absence of transplant rejection when there is a strong B cell response. Breg deficiencies have been reported in lupus, and the disappointing effects in this disease of treatments designed to inhibit the B cell response may be related to further Breg impairment. In several animal models, Breg stimulation is effective in correcting a variety of autoimmune disorders, most notably those initiated in the mucous membranes. Research into the interactions between the gut microbiota and Bregs holds considerable promise.
authors.affiliation: Service de rhumatologie, Hôtel-Dieu, CHU de Nantes, place Alexis-Ricordeau, 44093 Nantes cedex 01, France. jeanmarie.berthelot@chu-nantes.fr
authors.forename: Jean-Marie
authors.initials: JM
authors.lastname: Berthelot
authors.forename: Christophe
authors.initials: C
authors.lastname: Jamin
authors.forename: Kahina
authors.initials: K
authors.lastname: Amrouche
authors.forename: Benoit
authors.initials: B
authors.lastname: Le Goff
authors.forename: Yves
authors.initials: Y
authors.lastname: Maugars
authors.forename: Pierre
authors.initials: P
authors.lastname: Youinou
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000503:physiopathology*; D001402:B-Lymphocytes / Q000378:metabolism; D060151:B-Lymphocytes, Regulatory / Q000502:physiology*; D004195:Disease Models, Animal; D006801:Humans; D006967:Hypersensitivity / Q000503:physiopathology*; D007107:Immune System / Q000502:physiology / Q000503:physiopathology; D016753:Interleukin-10 / Q000378:metabolism*; D050378:T-Lymphocytes, Regulatory / Q000502:physiology*
chemical_list: D016753:Interleukin-10