Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1093/bjd/ljac048 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
B-Cell-Derived TGF-β1 Inhibits Osteogenesis and Contributes to Bone Loss in Periodontitis.
J Dent Res
July 2023
Department of Basic Science of Stomatology, Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing, China.
B cells play a vital role in the elimination of periodontal pathogens, the regulation of the immune response, and the induction of tissue destruction. However, the role of B cells in the dysfunction of mesenchymal stem cell (MSC) differentiation to osteoblasts in periodontitis (PD) has been poorly studied. Here we show that the frequency of CD45CD105CD73 MSCs in inflamed periodontal tissues is significantly decreased in patients with PD compared with that of healthy controls.
View Article and Find Full Text PDFB-cell-derived transforming growth factor-β may drive the activation of inflammatory macrophages and contribute to scarring in hidradenitis suppurativa.
Br J Dermatol
February 2023
The Charles Centre, Department of Dermatology and.
Expression of immunoglobulin G in human proximal tubular epithelial cells.
Mol Med Rep
May 2021
Department of Nephrology, Peking University Third Hospital, Beijing 100191, P.R. China.
Proximal tubular epithelial cells (PTECs) have innate immune characteristics, and produce proinflammatory factors, chemokines and complement components that drive epithelial‑mesenchymal transition (EMT). Our previous studies revealed that human mesangial cells and podocytes were able to synthesize and secrete immunoglobulin (Ig)A and IgG, respectively. The aim of the present study was to evaluate the expression of Igs in PTECs.
View Article and Find Full Text PDFActivation of human B cells negatively regulates TGF-β1 production.
J Neuroinflammation
January 2017
Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Background: Accumulating evidence indicate that B cells can exhibit pro- or anti-inflammatory activities. Similar to interleukin (IL)-10-competent B cells, we recently showed that transforming growth factor (TGF)-β1-producing regulatory B cells limit the induction of autoimmune neuroinflammation in mice, making them potentially important in maintaining peripheral immune tolerance in central nervous system inflammatory demyelinating disorders such as multiple sclerosis.
Methods: In this study, we compared B cell production of TGF-β1 and IL-10, the two most studied regulatory cytokines, and the pro-inflammatory B cell-derived IL-6 and tumor necrosis factor cytokines under basal conditions and following polyclonal stimulation with dual B cell receptor (BCR) cross-linking and Toll-like receptor (TLR)9 engagement.
B cell-derived transforming growth factor-β1 expression limits the induction phase of autoimmune neuroinflammation.
Sci Rep
October 2016
Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Studies in experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS), have shown that regulatory B cells modulate the course of the disease via the production of suppressive cytokines. While data indicate a role for transforming growth factor (TGF)-β1 expression in regulatory B cell functions, this mechanism has not yet been tested in autoimmune neuroinflammation. Transgenic mice deficient for TGF-β1 expression in B cells (B-TGF-β1) were tested in EAE induced by recombinant mouse myelin oligodendrocyte glycoprotein (rmMOG).
View Article and Find Full Text PDF