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01.12.2017 | Research article | Ausgabe 1/2017 Open Access

Arthritis Research & Therapy 1/2017

Excessive activation of the TLR9/TGF-β1/PDGF-B pathway in the peripheral blood of patients with systemic lupus erythematosus

Zeitschrift:
Arthritis Research & Therapy > Ausgabe 1/2017
Autoren:
Yi Yuan, Mingyue Yang, Kuo Wang, Jing Sun, Lili Song, Xue Diao, Zhenyu Jiang, Genhong Cheng, Xiaosong Wang
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​s13075-017-1238-8) contains supplementary material, which is available to authorized users.

Abstract

Background

Our aim is to study the existence of the TLR9/TGF-β1/PDGF-B pathway in healthy humans and patients with systemic lupus erythematosus (SLE), and to explore its possible involvement in the pathogenesis of lupus nephritis (LN).

Methods

Protein levels of the cytokines were detected by ELISA. mRNA levels of the cytokines were analyzed by real-time PCR. MTT assay was used to test the proliferation of mesangial cells under different treatments.

Results

Compared to healthy controls (N Control = 56), levels of Toll-like receptor (TLR)9, transforming growth factor (TGF)-β1, and platelet-derived growth factor B (PDGF-B) were increased significantly in the peripheral blood of SLE patients (N SLE = 112). Significant correlations between the levels of TLR9, TGF-β1, and PDGF-B were observed in both healthy controls and SLE patients. The levels of TGF-β1 and PDGF-B were greatly enhanced by TLR9 activation in primary cell cultures. The proliferation of mesangial cells induced by the plasma of SLE patients was significantly higher than that induced by healthy controls; PDGF-B was involved in this process. The protein levels of PDGF-B homodimer correlated with the levels of urine protein in SLE patients with LN (N LN =38).

Conclusions

The TLR9/TGF-β1/PDGF-B pathway exists in humans and can be excessively activated in SLE patients. High levels of PDGF-B may result in overproliferation of mesangial cells in the kidney that are involved in the development of glomerulonephritis and LN. Further studies are necessary to identify TLR9, TGF-β1, and PDGF-B as new therapeutic targets to prevent the development of glomerulonephritis and LN.
Zusatzmaterial
Additional file 1: Table S1. Clinical data of the study subjects. (XLS 23 kb)
13075_2017_1238_MOESM1_ESM.xls
Additional file 2: Figure S1. CpG induces upregulation of TGF-β1 and PDGF-B in monocytes in vitro. Isolated monocytes from healthy controls (A and B; N Control = 8) and SLE patients (C and D; N SLE = 7) were stimulated with or without 500 nM CpG for 24 h, and then mRNA expression of TGF-β1 and PDGF-B were detected by qPCR. Multiple rates of mRNA expression of TGF-β1 (E) and PDGF-B (F) in healthy controls (N Control = 8) and SLE patients (N SLE = 7) were calculated as CpG/Media. The results are presented as mean and SEM. (PPTX 510 kb)
13075_2017_1238_MOESM2_ESM.pptx
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