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1 ween plasmacytoid dendritic cells (pDCs) and Breg cells.
2 mablast differentiation but failed to induce Breg cells.
3 onditions reduces the number and function of Breg cells.
4 e the functional properties and phenotype of Breg cells?
6 B cells into IL-10-producing CD24(+)CD38(hi) Breg cells and plasmablasts, via the release of IFN-alph
8 used to induce autologous Breg and IL-35(+) Breg cells and treat autoimmune and inflammatory disease
15 ons to discuss the advances in understanding Breg cell biology, with a particular emphasis on their o
16 in vivo existence of allergen-specific human Breg cells comes from direct detection of their increase
23 ignaling (IL-12Rbeta2 KO mice) produced less Breg cells endogenously or after treatment with IL-35 an
27 ovel observations demonstrate a role for the Breg cell in germinal center reactions and suggest that
28 t microbiota promotes the differentiation of Breg cells in the spleen as well as in the mesenteric ly
29 induced by both the gut flora and arthritis, Breg cells increase in number and restrain excessive inf
31 opose that alteration in pDC-CD24(+)CD38(hi) Breg cell interaction contributes to the pathogenesis of
36 ve pDC-mediated expansion of CD24(+)CD38(hi) Breg cell numbers in SLE was associated with altered STA
42 autoimmune disease, and increased numbers of Breg cells prevent host defense to infection and promote
45 generation of regulatory T and regulatory B (Breg) cell responses; regulation of IgE and IgG4; decrea
46 on their ontogeny; we propose that multiple Breg cell subsets can be induced in response to inflamma
48 transforming growth factor beta (TGF-beta), Breg cells suppress immunopathology by prohibiting the e
49 terleukin-10 (IL-10)-producing regulatory B (Breg) cells suppress autoimmune disease, and increased n
51 induced the conversion of human B cells into Breg cells, these findings suggest that IL-35 may be use
52 flammatory signals in the differentiation of Breg cells, they also raise other questions about Breg c
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