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Excessive activation of the TLR9/TGF-?1/PDGF-B pathway in the peripheral blood of
patients with systemic lupus erythematosus
#MMPMID28356164
Yuan Y
; Yang M
; Wang K
; Sun J
; Song L
; Diao X
; Jiang Z
; Cheng G
; Wang X
Arthritis Res Ther
2017[Mar]; 19
(1
): 70
PMID28356164
show ga
BACKGROUND: Our aim is to study the existence of the TLR9/TGF-?1/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)-?1, 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-?1, and
PDGF-B were observed in both healthy controls and SLE patients. The levels of
TGF-?1 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-?1/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-?1, and PDGF-B as new therapeutic targets to prevent the
development of glomerulonephritis and LN.
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