Kidney Expression of Toll Like Receptors in Lupus Nephritis: Quantification and Clinicopathological Correlations. (21st August 2016)

• Record Type: Journal Article
• Authors: Conti, Fabrizio; Spinelli, Francesca Romana; Truglia, Simona; Miranda, Francesca; Alessandri, Cristiano; Ceccarelli, Fulvia; Bombardieri, Michele; Giannakakis, Konstantinos; Valesini, Guido
• Other Names: Zelante Teresa Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2016(2016)
• Publication Date: 2016-08-21
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2016/7697592
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Objective . The study aimed at locating and quantifying Toll Like Receptor (TLR) 3, 7, 8, and 9 expression in kidney of patients with lupus nephritis (LN) and correlating them with clinicopathological features. Methods . Kidney sections from 26 LN patients and 4 controls were analyzed by immunohistochemistry using anti-human TLR3, TLR7, TLR8, and TLR9 polyclonal antibodies; the number of TLR-positive nuclei/mm 2 was evaluated on digitalized images. Results . Compared to controls, LN showed a significantly higher amount of glomerular and tubulointerstitial TLR9 (p = 0.003 andp = 0.007 ), whole and tubulointerstitial TLR3 (p = 0.026 andp = 0.031 ), and a higher tubulointerstitial TLR7 (p = 0.022 ). TLR9 positively correlated with activity index (p = 0.0063 ) and tubular TLR7 with chronicity index (p = 0.026 ). TLR9 positively correlated with Renal-SLEDAI (p = 0.01 ). Conclusions . This is the first study quantifying kidney expressions of TLRs in LN patients; the results show an overexpression of TLR3, TLR7, and TLR9 and demonstrate a correlation with clinicopathological indices supporting a role of these mediators in the pathogenesis of LN.