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Suppressors of cytokine signalling in ankylosing spondylitis and their associations with disease severity, acute-phase reactants and serum cytokines


1, 2, 3, 4, 5, 6

 

  1. Division of Allergy, Immunology and Rheumatology, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taiwan, and School of Medicine, Tzu Chi University, Hualien; and Taipei Medial University, and Municipal Wan Fang Hospital, Taipei, Taiwan.
  2. Chi Mei Medical Center, Tainan, Taiwan.
  3. Taipei Medical University, and Municipal Wan Fang Hospital, Taipei, Taiwan.
  4. Division of Allergy, Immunology and Rheumatology, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taiwan, and School of Medicine, Tzu Chi University, Hualien, Taiwan.
  5. National Yang-Ming University, and Taipei Veterans General Hospital, Taipei, Taiwan.
  6. National Yang-Ming University, and Taipei Veterans General Hospital, Taipei, Taiwan. ctchou@vghtpe.gov.tw

CER8271
2016 Vol.34, N°1
PI 0100, PF 0105
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PMID: 26812031 [PubMed]

Received: 08/01/2015
Accepted : 04/09/2015
In Press: 20/01/2016
Published: 10/02/2016

Abstract

OBJECTIVES:
To investigate the suppressors of cytokine signalling (SOCS1 and SOCS3) expression in peripheral blood cells in ankylosing spondylitis (AS), and their associations with clinical and laboratory manifestations.
METHODS:
The levels of SOCS1 and SOCS3 mRNA in peripheral blood mononuclear cells (PBMCs), T cells and monocytes were measured by RT-PCR in 53 AS patients and 31 healthy controls. Patient’s serum IL-6, IL-10 and IL-17A levels were determined by ELISA. We evaluated patient’s disease activity, functional ability and global assessment, and tested their ESR, CRP and IgA levels.
RESULTS:
Cellular SOCS1 expression did not show significant differences between AS patients and controls. However, T cells SOCS1 decreased significantly in the AS subgroup with lower ESR than controls (p=0.013). PBMCs (p=0.047) and T cells (p=0.035) SOCS1 decreased significantly in the AS subgroup with lower CRP than controls. Importantly, SOCS3 expression increased significantly in AS patients compared to the controls in PBMCs (p=0.025), T cells (p=0.003) and monocytes (p=0.009). Moreover, PBMCs SOCS3 correlated with ESR (r=0.297, p=0.031) and CRP (r=0.320, p=0.019). T cells SOCS3 correlated with BASFI (r=0.337, p=0.015), ESR (r=0.435, p=0.001) and CRP (r=0.300, p=0.029). Monocytes SOCS3 correlated with ESR (r=0.281, p=0.041) and IgA (r=0.426, p=0.006). Furthermore, T cells SOCS1 (r=-0.454, p=0.023) and T cells SOCS3 (r=-0.405, p=0.045) negatively correlated with serum IL-17A. Monocytes SOCS3 negatively correlated with serum IL-6 (r=-0.584, p=0.002).
CONCLUSIONS:
The decreased SOCS1 and increased SOCS3 expression in AS PBMCs and T cells, and their correlation with patient’s functional ability, acute-phase reactants and serum pro-inflammatory cytokines suggested that SOCS may participate in the pathogenesis of AS.

Rheumatology Article