Role of Genetic Predisposition, Cytokines, and Neuroendocrine Response in Development of Thyroid Autoimmunity

Cytokines ◽  
2006 ◽  
pp. 396-407
Keyword(s):  
Genetic Predisposition ◽  
Thyroid Autoimmunity ◽  
Neuroendocrine Response

The Th1/Th2 paradigm in thyroid autoimmunity: the role of CXCR6+ T-cells

2004 ◽  
Vol 112 (S 1) ◽  
Author(s):  
G Aust ◽  
M Kamprad ◽  
D Sittig ◽  
L Becherer ◽  
P Lamesch ◽  
...  
Keyword(s):  
T Cells ◽  
Thyroid Autoimmunity

Association of genetic polymorphism of cytokines and antioxidant enzymes with the development of asbestosis

2020 ◽  
Vol 60 (12) ◽  
pp. 898-903
Author(s):  
Lyudmila P. Kuzmina ◽  
Anastasiya G. Khotuleva ◽  
Evgeniy V. Kovalevsky ◽  
Nikolay N. Anokhin ◽  
Iraklij M. Tskhomariya
Keyword(s):  
Antioxidant Enzymes ◽  
Genetic Polymorphism ◽  
Genetic Predisposition ◽  
Risk Groups ◽  
Dust Exposure ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Gstp1 Gene ◽  
Polymorphic Variants

Introduction. Various industries widely use chrysotile asbestos, which determines the relevance of research aimed at the prevention of asbestos-related diseases. It is promising to assess the role of specific genes, which products are potentially involved in the development and regulation of certain links in the pathogenesis of asbestosis, forming a genetic predisposition to the disease. The study aims to analyze the presence of associations of genetic polymorphism of cytokines and antioxidant enzymes with asbestosis development. Materials and methods. Groups were formed for examination among employees of OJSC "Uralasbest" with an established diagnosis of asbestosis and without lung diseases. For each person included in the study, dust exposure doses were calculated considering the percentage of time spent at the workplace during the shift for the entire work time. Genotyping of single nucleotide polymorphisms of cytokines IL1b (rs16944), IL4 (rs2243250), IL6 (rs1800795), TNFα (rs1800629) and antioxidant enzymes SOD2 (rs4880), GSTP1 (rs1610011), CAT (rs1001179) was carried out. Results. The authors revealed the associations of polymorphic variants A511G IL1b gene (OR=2.457, 95% CI=1.232-4.899) and C47T SOD2 gene (OR=1.705, 95% CI=1.055-2.756) with the development of asbestosis. There was an increase in the T allele IL4 gene (C589T) frequency in persons with asbestosis at lower values of dust exposure doses (OR=2.185, 95% CI=1.057-4.514). The study showed the associations of polymorphism C589T IL4 gene and C174G IL6 gene with more severe asbestosis, polymorphism A313G GSTP1 gene with pleural lesions in asbestosis. Conclusion. Polymorphic variants of the genes of cytokines and antioxidant enzymes, the protein products directly involved in the pathogenetic mechanisms of the formation of asbestosis, contribute to forming a genetic predisposition to the development and severe course of asbestosis. Using the identified genetic markers to identify risk groups for the development and intense period of asbestos-related pathology will optimize treatment and preventive measures, considering the organism's characteristics.

Role of the Specialized Pro-resolving Mediator Resolvin D1 in Hashimotoʼs Thyroiditis

2021 ◽  
Author(s):  
Jing Song ◽  
Rongxin Sun ◽  
Yuanyuan Zhang ◽  
Ying Fu ◽  
Dong Zhao
Keyword(s):  
Thyroid Autoimmunity ◽  
Thyroid Stimulating Hormone ◽  
Inflammatory Factors ◽  
Thyroid Peroxidase ◽  
Sensitivity Index ◽  
Resolvin D1 ◽  
Thyroid Peroxidase Antibody ◽  
Thyroglobulin Antibody ◽  
Inflammation Resolution

Abstract Objective Resolvins are produced by the catabolism of polyunsaturated fatty acids (PUFAs) and play vital roles in inflammation resolution. Resolvins have been associated with autoimmune disorders. This study aimed to measure the level of Resolvin D1 (RVD1) in the serum of Hashimoto's thyroiditis (HT) patients and healthy controls (HCs) and to further analyse its correlation with thyroid autoantibodies and inflammatory factors. Methods Sixty-three participants were recruited, namely, 30 untreated HT patients and 33 sex- and age-matched HCs. Serum RVD1 and inflammatory chemokine (MCP-1 and IP-10) levels were measured by ELISA according to the manufacturer’s protocol. Serum total T3 (TT3), TT4, free T3 (FT3), FT4, thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb) and thyroid-stimulating hormone (TSH) levels were measured using an electrochemiluminescence immunoassay. Thyroid homeostasis parameters, including the thyroid secretory capacity (SPINA-GT), the total deiodinase activity (SPINA-GD), Jostel’s TSH index (TSHI) and the thyrotroph thyroid hormone sensitivity index (TTSI), were calculated. Results Serum RVD1 levels in HT patients (134.76, 85.35–201.36 pg/mL) were significantly lower than those in HCs (187.64, 131.01–326.85 pg/mL) (P=0.004). As the TPOAb level increased, the RVD1 level showed a decreasing trend (P for trend=0.002). Both multinomial and ordinal logistics analyses revealed that serum RVD1 levels were negatively correlated with TPOAb levels in the adjusted models. Moreover, RVD1 showed a negative correlation with the inflammatory chemokine IP-1 0 (r=–0.276, P=0.034), TSHI (r=–0.269, P=0.036) and TTSI (r=–0.277, P=0.031). Conclusions Thyroid autoimmunity may be associated with low levels of RVD1. Decreased RVD1 levels indicate impaired resolution of inflammation in HT patients.

Congenital hypothyroidism in a Turkish family: the role of immunoglobulins blocking the trophic effects of TSH and maternal-foetal relationship

1986 ◽  
Vol 111 (1) ◽  
pp. 44-53 ◽  
Author(s):  
R. D. van der Gaag ◽  
H. Frisch ◽  
M. Weissel ◽  
G. Wick ◽  
H. A. Drexhage
Keyword(s):  
Congenital Hypothyroidism ◽  
Thyroid Autoimmunity ◽  
Thyroid Tissue ◽  
Mild Form ◽  
Juvenile Form ◽  
Turkish Family ◽  
Blocking Antibodies ◽  
Thyroid Microsomal Antibodies ◽  
Trophic Action

Abstract. A Turkish family with frequent intermarriages is described, in which two siblings were born with persistent forms of congenital hypothyroidism, in the elder child concomitant with absent radioactive thyroid imaging. The mother was clinically euthyroid throughout the period of observation, but showed in addition to thyroid microsomal antibodies, high levels of immunoglobulins blocking the trophic action of TSH. These maternal growth blocking antibodies were transiently present in the youngest of the siblings (from birth to 2 months of age). She had a relatively mild form of congenital hypothyroidism (T3: 33 μg/100 ml; T4: 3.9 μg/100 ml). The older sibling, with proven non-functioning thyroid tissue (negative thyroidscan, T4: 0.4 μg/100 ml) produced the growth-blocking immunoglobulins herself and may thus represent a juvenile form of thyroid autoimmunity with a very early onset. An aunt and uncle of the children, both hypothyroid since birth, were at the age of 19 and 18 years weakly positive for growth blocking immunoglobulins. This study indicates that familial forms of congenital hypothyroidism are probably complex and may be brought about by maternal to foetal passage of thyroid reactive autoantibodies, but also by the inheritance of a trait for thyroid autoimmunity. In some cases these two mechanisms might act in conjunction.

Role of Nitric Oxide in the Neuroendocrine Response to Cytokines

2001 ◽  
pp. 117-129 ◽  
Author(s):  
S.M. McCann ◽  
M. Kimura ◽  
S. Karanth ◽  
W.H. Hu ◽  
V. Rettori
Keyword(s):  
Nitric Oxide ◽  
Neuroendocrine Response

scholarly journals The Role of Thyroid Hormones and Autoantibodies in Metabolic Dysfunction Associated Fatty Liver Disease: TgAb May Be a Potential Protective Factor

2020 ◽  
Vol 11 ◽  
Author(s):  
Xiaofu Zhang ◽  
Ruyi Li ◽  
Yingjie Chen ◽  
Yuning Dai ◽  
Ling Chen ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Liver Disease ◽  
Fatty Liver Disease ◽  
Protective Factor ◽  
Thyroid Autoimmunity ◽  
Metabolic Dysfunction ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tsh Levels

BackgroundPrevious studies have shown that metabolic dysfunction associated fatty liver disease (MAFLD) is associated with thyroid hormones (THs), immunity, and inflammation status, but few studies involved thyroid autoimmunity. This study aimed to evaluate the role of THs, thyroid autoantibodies, inflammatory biomarkers in MAFLD, its cofactors, and other possible determinants.Materials and MethodsIn the study, a total of 424 Chinese patients were selected and categorized as non-MAFLD and MAFLD. Serum thyroid hormone, thyroid autoantibody and high-sensitive C-reactive protein (hsCRP) levels were measured. The data of blood pressure, the serum lipid profile, glucose and liver enzymes were collected. The differences and association between research findings were examined and analyzed by Wilcoxon Signed Rank Test, One-Way ANOVA test and Multiple Logistic Regression models.ResultsThe study showed significant increase in the prevalence of MAFLD with high thyroid stimulating hormone (TSH) levels (P < 0.01) and abnormal high-sensitive C-reactive protein (hsCRP) levels (P < 0.01). The proportion of MAFLD patients decreased significantly with the rise of free thyroxine (FT4) (P = 0.04), thyrotropin receptor antibodies (TRAb) (P < 0.01), anti-thyroglobulin antibodies (TgAb) (P < 0.01), and thyroid peroxidase antibodies (TPOAb) levels (P < 0.01). Based on logistic regression analysis, MAFLD was significantly associated with lower levels of TgAb (P < 0.01), TPOAb (P < 0.01), and higher levels of hsCRP (P < 0.01) in male. In female, elevated TgAb (P < 0.01) may be a protective factor, while higher levels of hsCRP (P < 0.01) showed increased risk of MAFLD. Logistic models were adjusted for age, BMI, SBP, DBP, FBG, ALT, AST, TC, TG, LDL, HDL.ConclusionsTaken together, TgAb may be a potential protective factor for MAFLD and elevated hsCRP level should be considered as an independent risk factor for MAFLD in both genders. TPOAb also demonstrated protective effect, but only in male. The prevalence of MAFLD increased with higher TSH levels and lower FT4, TRAb levels, but no significant association were found. However, Our findings provide a new insight into the pathogenesis of MAFLD by further investigating the impact of THs, thyroid autoimmunity, and inflammation on MAFLD patients.

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