コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ween plasmacytoid dendritic cells (pDCs) and Breg cells.
2 T cell-dependent inflammatory response into Breg cells.
3 mablast differentiation but failed to induce Breg cells.
4 plasmablasts, and IL-10(+) and/or IL-1RA(+) Breg cells.
5 onditions reduces the number and function of Breg cells.
6 e the functional properties and phenotype of Breg cells?
7 ll subsets shows that GA-dependent increased Breg cell activities are specifically supported by the B
9 induces both human and mouse IL-10-producing Breg cells and increases their survival with a concomita
10 B cells into IL-10-producing CD24(+)CD38(hi) Breg cells and plasmablasts, via the release of IFN-alph
12 the regulatory properties of a new brand of Breg cells and provided mechanistic insights into potent
13 used to induce autologous Breg and IL-35(+) Breg cells and treat autoimmune and inflammatory disease
14 t SLAMF5 is a negative moderator of IL-10(+) Breg cells, and may serve as a therapeutic target in MS
17 CD19(+)CD73(-)CD25(+)CD71(+)TIM-1(+)CD154(+) Breg cells are enriched in the peripheral blood of human
22 and desensitized groups, B cell activation-, Breg cells-, BCR-signaling-, and differentiation-related
24 ons to discuss the advances in understanding Breg cell biology, with a particular emphasis on their o
25 in vivo existence of allergen-specific human Breg cells comes from direct detection of their increase
29 asmablast differentiation, and regulatory B (Breg) cell development during allergen-specific immunoth
33 ignaling (IL-12Rbeta2 KO mice) produced less Breg cells endogenously or after treatment with IL-35 an
36 this review, we discuss immunobiology of i35-Breg cell, i35-Breg therapies for autoimmune diseases an
38 ovel observations demonstrate a role for the Breg cell in germinal center reactions and suggest that
39 could be a useful therapy for recovering the Breg cells in autoimmune situations in which their activ
40 t microbiota promotes the differentiation of Breg cells in the spleen as well as in the mesenteric ly
41 ts have shown the ability to induce Treg and Breg cells in vivo which may have potential importance f
42 e control of the activities of regulatory B (Breg) cells in immune disorders is an emerging therapeut
43 induced by both the gut flora and arthritis, Breg cells increase in number and restrain excessive inf
45 opose that alteration in pDC-CD24(+)CD38(hi) Breg cell interaction contributes to the pathogenesis of
50 ve pDC-mediated expansion of CD24(+)CD38(hi) Breg cell numbers in SLE was associated with altered STA
56 autoimmune disease, and increased numbers of Breg cells prevent host defense to infection and promote
60 generation of regulatory T and regulatory B (Breg) cell responses; regulation of IgE and IgG4; decrea
61 IL-10(+) and dual-positive IL-10(+)IL-1RA(+) Breg cells significantly correlated with improved clinic
62 on their ontogeny; we propose that multiple Breg cell subsets can be induced in response to inflamma
64 transforming growth factor beta (TGF-beta), Breg cells suppress immunopathology by prohibiting the e
65 terleukin-10 (IL-10)-producing regulatory B (Breg) cells suppress autoimmune disease, and increased n
67 quality control measures to deliver a viable Breg-cell therapy product for administration to a transp
69 induced the conversion of human B cells into Breg cells, these findings suggest that IL-35 may be use
70 flammatory signals in the differentiation of Breg cells, they also raise other questions about Breg c
72 smablasts and IL-10- and/or IL-1RA-producing Breg cells was greater among responders compared with no
75 IL-1 receptor antagonist (IL-1RA)-producing Breg cells were investigated and correlated to clinical