Evaluation of MIF -173 G/C Polymorphism in Turkish Patients with Ankylosing Spondylitis

Gürel, Çevik; Inanir, Ahmet; Nursal, Ayşe Feyda; Tekcan, Akın; Rüstemoğlu, Aydın; Yığıt, Serbülent

doi:10.5152/balkanmedj.2016.141103

Cited by 5 publications

(3 citation statements)

References 28 publications

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“…Hypermethylation of both p14 ARF and p16 INK4a was found in normal colonic mucosal tissues of patients with UC, as well in the precancerous lesions, suggesting that UC patients with this particular inflammatory genotype of MIF may be at a higher risk for developing colonic cancer (128). This rs755622C genotype association was also observed in patients with IBD and in Chinese patients with psoriasis, but not in Turkish patients with AS (97,98,129). Despite that, the authors have suggested that the time of onset and the duration of AS still might be affected by rs755622C allele (129).…”

Section: Suggested Novel Hypothesismentioning

confidence: 83%

“…This rs755622C genotype association was also observed in patients with IBD and in Chinese patients with psoriasis, but not in Turkish patients with AS (97,98,129). Despite that, the authors have suggested that the time of onset and the duration of AS still might be affected by rs755622C allele (129). However, this hypothesis still needs to be proven in the laboratory, along with testing for MIF-rs755622C allele in more patients with early-onset jSpA.…”

Section: Suggested Novel Hypothesismentioning

confidence: 93%

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Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

Harjaček

2021

Front. Med.

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Juvenile spondyloarthritis (jSpA) is a an umbrella term for heterogeneous group of related seronegative inflammatory disorders sharing common symptoms. Although it mainly affects children and adolescents, it often remains active during adulthood. Genetic and environmental factors are involved in its occurrence, although the exact underlying immunopathophysiology remains incompletely elucidated. Accumulated evidence suggests that, in affected patients, subclinical gut inflammation caused by intestinal dysbiosis, is pivotal to the future development of synovial–entheseal complex inflammation. While the predominant role of IL17/23 axis, TNF-α, and IL-7 in the pathophysiology of SpA, including jSpA, is firmly established, the role of the cytokine macrophage migration inhibitory factor (MIF) is generally overlooked. The purpose of this review is to discuss and emphasize the role of epigenetics, neuroendocrine pathways and the hypothalamic-pituitary (HPA) axis, and to propose a novel hypothesis of the role of decreased NLRP3 gene expression and possibly MIF in the early phases of jSpA development. The decreased NLRP3 gene expression in the latter, due to hypomethylation of promotor site, is (one of) the cause for inflammasome malfunction leading to gut dysbiosis observed in patients with early jSpA. In addition, we highlight the role of MIF in the complex innate, adaptive cellular and main effector cytokine network, Finally, since treatment of advanced bone pathology in SpA remains an unmet clinical need, I suggest possible new drug targets with the aim to ultimately improve treatment efficacy and long-term outcome of jSpA patients.

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Section: Suggested Novel Hypothesismentioning

confidence: 83%

Section: Suggested Novel Hypothesismentioning

confidence: 93%

Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

Harjaček

2021

Front. Med.

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“…Two databases were about atopic dermatitis (AD) [25,26], Henoch-Schonlein purpura nephritis (HSPN) [27], and Henoch-Schonlein purpura (HSP) [28]. The other nine diseases were inquired in single databases, including ankylosing spondylitis (AS) [29], primary gout [30], primary biliary cirrhosis (PBC) [24], psoriasis (Ps) [31], systemic lupus erythematosus (SLE) [32], Vogt-Koyanagi-Harada syndrome (VKH) [33], adult still disease (AOSD) [34], Behcet's disease (BD) [35], and scleroderma (SD) [36]. The areas of the studies involved in the present analysis were Asian, Europe, and North America.…”

Section: Characteristics Of Eligible Studiesmentioning

confidence: 99%

The Role of MIF-173G/C Gene Polymorphism in the Susceptibility of Autoimmune Diseases

Song

et al. 2020

Mediators of Inflammation

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Some certain genetic polymorphisms have been considered to implicate in the pathogenesis and progression of autoimmune diseases and may predispose to an early stage of general autoimmune susceptibility. Recent studies have been conducted to investigate the association between macrophage migration inhibitory factor- (MIF-) 173G/C gene polymorphism and autoimmune diseases; however, the results were not exactly identical. In the present study, a systematic review and meta-analysis of case-control studies was performed to estimate the relationship. A comprehensive search of PubMed, Ebsco, EMbase, WanFang databases and CNKI was done. Odds ratio (ORs) and corresponding 95% confidence intervals (CIs) were combined to pool the effect size. The publication bias was examined by Begg’s funnel plots and Egger’s test. RevMan 5.3 and STATA 12.0 software were used for statistical processing. 23 papers were included, and the results revealed that MIF-173G/C was significantly associated with an increased risk of autoimmune diseases in five genetic models (recessive genetic model: OR=1.95, 95% CI: 1.52-2.50; dominant genetic model: OR=1.35, 95% CI: 1.24-1.46; allele model: OR=1.32, 95% CI: 1.23-1.41; homozygote model: OR=1.92, 95% CI: 1.57-2.35; heterozygote model: OR=4.92, 95% CI: 4.03-6.02), whether in Asia, Europe, or North America. Furthermore, subgroup analysis showed an increasing risk in rheumatoid arthritis (RA), ulcerative colitis (UC), Crohn’s disease (CD), atopic dermatitis (AD), Henoch-Schonlein purpura (HSP), and Henoch-Schonlein purpura nephritis (HSPN), but it was not related to the susceptibility of autoimmune hepatitis (AIH). Therefore, it could be considered that MIF-173G/C polymorphism could increase the susceptibility of autoimmune diseases, while there may be the discrepancy of disease entity.

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Association of Non-HLA Genes with Ankylosing Spondylitis

Rahmati

Hakemi

2021

Ankylosing Spondylitis - Axial Spondyloarthritis

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Evaluation of MIF -173 G/C Polymorphism in Turkish Patients with Ankylosing Spondylitis

Cited by 5 publications

References 28 publications

Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

The Role of MIF-173G/C Gene Polymorphism in the Susceptibility of Autoimmune Diseases

Association of Non-HLA Genes with Ankylosing Spondylitis

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