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Ankylosing Spondylitis M-Csf-Derived Macrophages Are Undergoing Unfolded Protein Response (Upr) and Express Higher Levels of Interleukin-23 Publisher Pubmed



Rezaiemanesh A1 ; Mahmoudi M2 ; Amirzargar AA1, 3 ; Vojdanian M2 ; Jamshidi AR2 ; Nicknam MH1, 3
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran

Source: Modern Rheumatology Published:2017


Abstract

Objective: Interleukin (IL)-23/IL-17 pathway involves in the pathogenesis of ankylosing spondylitis (AS). The exact mechanism implicated in overexpression of IL-23 and activation of the IL-23/IL-17 axis is not clear. The aim of the study was to clarify whether macrophages of AS patients undergo unfolded protein response (UPR) and secret increased IL-23. Methods: Peripheral blood monocyte isolated from 10 HLA-B27+ patients and five HLA-B27+ normal subjects were differentiated to macrophages by macrophage-colony stimulating factor (M-CSF) for seven days. Flow cytometry was used to detect monocyte purity and expression of macrophage markers. Analysis of mRNA expression for HLA-B and B27, UPR-associated proteins (BiP, CHOP, MDG1, and XBP1) and IL-23 was performed by RT-qPCR. Results: RT-qPCR data showed a significant overexpression of HLA-B27, UPR genes (BiP, CHOP, and XBP1), and IL-23 in M-CSF-derived macrophages from AS patients compared to healthy controls. Increased expression of MDG1 was not significant. Conclusions: Our data suggest that UPR activation occurs in M-CSF-derived macrophages of AS patients and is accompanied by overexpression of HLA-B27. UPR appears to be associated with overproduction of IL-23 in AS macrophages. © 2016 Japan College of Rheumatology.
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