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Suppressors of cytokine signalling in ankylosing spondylitis and their associations with disease severity, acute-phase reactants and serum cytokines
C.-H. Chen1, H.-A. Chen2, H.-T. Liao3, C.-H. Liu4, C.-Y. Tsai5, C.-T. Chou6
- 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.
- Chi Mei Medical Center, Tainan, Taiwan.
- Taipei Medical University, and Municipal Wan Fang Hospital, Taipei, Taiwan.
- 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.
- National Yang-Ming University, and Taipei Veterans General Hospital, Taipei, Taiwan.
- 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.