scholarly journals Macrophage Migration Inhibitory Factor Interacting with Th17 Cells May Be Involved in the Pathogenesis of Autoimmune Damage in Hashimoto’s Thyroiditis

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Haibo Xue ◽  
Yuhua Yang ◽  
Ying Zhang ◽  
Shoujun Song ◽  
Li Zhang ◽  
...  

Purpose. To explore the possible role of MIF and Th17 cells in the thyroid-specific autoimmune damage of Hashimoto’s thyroiditis (HT).Material and Methods. We enrolled 40 HT patients and 30 healthy controls and divided HT patients into euthyroid subset (n=22) and subclinical or overt hypothyroidism subset (n=18). The percentages of Th17 cells and expressions of MIF, interleukin 17A (IL-17A) mRNA in PBMCs, as well as serum concentrations of MIF, and IL-17A, and thyroid functions, and thyroid-specific autoantibodies (TPOAb, TgAb) were detected by flow cytometry, real-time RT-PCR, ELISA, and ECLIA in all subjects.Results. MIF mRNA, IL-17A mRNA expressions and Th17 cells percentages, serum MIF, and IL-17A protein levels were all significantly higher in HT patients, even in euthyroid subgroup. Additionally, the differences became more obvious in dysfunction subgroup. Importantly, both MIF levels and Th17 cells percentage were positively correlated with serum TPOAb, TgAb, and thyrotropin (TSH) levels in HT patients.Conclusions. These data suggest that MIF and Th17 cells increased dynamically and positively correlated with the markers of thyroid autoimmune damage, which indicated that interaction between MIF and Th17 cells may participate in the pathogenesis and development of thyroid-specific autoimmunity in HT.

2018 ◽  
Vol 15 (3) ◽  
pp. 128
Author(s):  
Devi Dayal ◽  
Sandhya Cautha ◽  
Naresh Sachdeva ◽  
Darshan Badal ◽  
SavitaVerma Attri ◽  
...  

2018 ◽  
Author(s):  
B Ramesh ◽  
B Rajesh ◽  
Reddy B Rajkiran ◽  
G Gayathri ◽  
Reddy M Venkateshwara ◽  
...  

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Ming Liu ◽  
Zikun Xie ◽  
Guang Sun ◽  
Liujun Chen ◽  
Dake Qi ◽  
...  

Abstract Background Osteoarthritis (OA) is the most prevalent form of arthritis and the major cause of disability and overall diminution of quality of life in the elderly population. Currently there is no cure for OA, partly due to the large gaps in our understanding of its underlying molecular and cellular mechanisms. Macrophage migration inhibitory factor (MIF) is a procytokine that mediates pleiotropic inflammatory effects in inflammatory diseases such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS). However, data on the role of MIF in OA is limited with conflicting results. We undertook this study to investigate the role of MIF in OA by examining MIF genotype, mRNA expression, and protein levels in the Newfoundland Osteoarthritis Study. Methods One hundred nineteen end-stage knee/hip OA patients, 16 RA patients, and 113 healthy controls were included in the study. Two polymorphisms in the MIF gene, rs755622, and -794 CATT5-8, were genotyped using polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) and PCR followed by automated capillary electrophoresis, respectively. MIF mRNA levels in articular cartilage and subchondral bone were measured by quantitative polymerase chain reaction. Plasma concentrations of MIF, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) were measured by enzyme-linked immunosorbent assay. Results rs755622 and -794 CATT5-8 genotypes were not associated with MIF mRNA or protein levels or OA (all p ≥ 0.19). MIF mRNA level in cartilage was lower in OA patients than in controls (p = 0.028) and RA patients (p = 0.004), while the levels in bone were comparable between OA patients and controls (p = 0.165). MIF protein level in plasma was lower in OA patients than in controls (p = 3.01 × 10−10), while the levels of TNF-α, IL-6 and IL-1β in plasma were all significantly higher in OA patients than in controls (all p ≤ 0.0007). Multivariable logistic regression showed lower MIF and higher IL-1β protein levels in plasma were independently associated with OA (OR per SD increase = 0.10 and 8.08; 95% CI = 0.04–0.19 and 4.42–16.82, respectively), but TNF-α and IL-6 became non-significant. Conclusions Reduced MIF mRNA and protein expression in OA patients suggested MIF might have a protective role in OA and could serve as a biomarker to differentiate OA from other joint disorders.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Aleksandra Pyzik ◽  
Ewelina Grywalska ◽  
Beata Matyjaszek-Matuszek ◽  
Jacek Roliński

This review of literature attempts to identify the factors that are involved in the pathogenesis of Hashimoto thyroiditis, an immune defect in an individual with genetic susceptibility accompanied with environmental factors. The frequency of Hashimoto’s disease is a growing trend and among Caucasians it is estimated at approximately 5%. The dysfunction of the gland may be clinically evident (0.1–2% of the population) or subclinical (10–15%). The pathology is diagnosed five to ten times more often in women than men and its incidence increases with the age (the peak of the number of cases is between 45 and 65); however, it can also be diagnosed in children. The pathogenesis of Hashimoto’s thyroiditis is still not fully comprehended. In the etiology of Hashimoto thyroiditis excessively stimulated T CD4+ cells are known to play the most important role. Recent research has demonstrated an increasing role of newly discovered cells such as Th17 (CD4+IL-17+) or T regulatory cells (CD4+CD25+highFoxP3+) in the induction of autoimmune disorders. The process of programmed cell death also plays an equally important role in the pathogenesis and the development of hypothyroidism.


2018 ◽  
Vol 44 (6) ◽  
pp. 1164-1169 ◽  
Author(s):  
Zi-mei Lin ◽  
Yao Wang ◽  
Chun-mei Liu ◽  
Cao-xin Yan ◽  
Pin-tong Huang

2015 ◽  
Vol 11 (02) ◽  
pp. 85 ◽  
Author(s):  
Liliana R Santos ◽  
Paulo Fonseca ◽  
Rita Cardoso ◽  
Paula Soares ◽  
◽  
...  

Hashimoto’s thyroiditis (HT) is the most common cause of hypothyroidism in adolescence and mainly affects females. Being the archetype of an organ-specific T-cell-mediated disease, it is characterized by lymphocytic infiltration of the thyroid gland, damage to the thyroid follicular cells, and impaired ability to produce thyroid hormones. It may be associated with other autoimmune diseases and may arise in the context of congenital chromosomal aberrations. Symptoms of hypothyroidism develop insidiously. In adolescents the most common manifestation is the increase of the glandular volume. Hypothyroidism manifestations (asthenia, intolerance to cold, constipation, and/or skin and dry hair) are less common. The diagnosis is based on the presence of thyroid antibodies and characteristic imaging abnormalities on thyroid ultrasound. The treatment relies on the administration of synthetic thyroid hormones for patients with overt hypothyroidism or subclinical hypothyroidism and significant goiter.


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