Immunological aspects of autoimmune thyroid disease – Complex interplay between cells and cytokines

Luty, Justyna; Rückemann-Dziurdzińska, Katarzyna; Witkowski, Jacek M.; Bryl, Ewa

doi:10.1016/j.cyto.2019.01.003

Cited by 60 publications

(63 citation statements)

References 37 publications

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“…We had no information on multiple AIDs in the spousal pairs because the study was limited to the first incident AID in each individual. Autoimmune thyroid diseases are known to have many environmental triggers and contributing factors, including infections, dietary iodine, selenium and polyhalogenatated environmental contaminants, which can interfere with thyroid function; spouses may also share dramatic psychosocial events [ 5 , 6 , 27 ]. Consanguinity would be an unlikely explanation of spousal sharing because the population is outbred.…”

Section: Discussionmentioning

confidence: 99%

“…For both diseases genetic and environmental causes are thought to be important. Microbial antigenes may be triggers of these diseases, as well as some dramatic psychosocial events [ 5 , 6 ]. Autoimmune thyroid diseases also appear as a side-effect of immunotherapy, which has recently become a promising novel therapeutic modality in the treatment of some cancers [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

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Familial risks between Graves disease and Hashimoto thyroiditis and other autoimmune diseases in the population of Sweden

Thomsen

Sundquist

et al. 2020

Journal of Translational Autoimmunity

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Genetic and family studies have indicated that Graves disease and Hashimoto thyroiditis have a heritable component which appears to be shared to some extend also with some other autoimmune diseases (AIDs). In the present nation-wide study we describe familial risk for Graves disease and Hashimoto thyroiditis identified from the Swedish Hospital Discharge Register (years 1964 through 2012) and the Outpatient Register (2001 through 2012). Family relationships were obtained from the Multigeneration Register and cancers from the Cancer Registry. Familial standardized incidence ratios (SIRs) were calculated for 29,005 offspring with Graves disease and for 25,607 offspring with Hashimoto thyroiditis depending on any of 43 AIDs in parents or siblings. The concordant familial risks for Graves disease and Hashimoto thyroiditis were 3.85 and 4.75, higher for men than for women. The familial risks were very high (11.35, Graves and 22.06, Hashimoto) when both a parent and a sibling were affected. Spousal familial risks were higher for Hashimoto thyroiditis (1.98/1.93) than for Graves disease (1.48/1.50). For Graves disease, 24 discordant AIDs showed a significant association; for Hashimoto thyroiditis, 20 discordant associations were significant. All significant discordant associations were positive for the two thyroid AIDs, with the exception of Hashimoto thyroiditis with Reiter disease. Overall 8 associations were significant only for Graves disease and 6 Hashimoto thyroiditis. The overall high concordant familial risks for Graves disease and Hashimoto thyroiditis suggest a strong genetic contribution to the familial risk. Significant familial associations among more than half of the 43 AIDs attest to the extensive polyautoimmunity among thyroid AIDs.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Familial risks between Graves disease and Hashimoto thyroiditis and other autoimmune diseases in the population of Sweden

Thomsen

Sundquist

et al. 2020

Journal of Translational Autoimmunity

View full text Add to dashboard Cite

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“…In support of this hypothesis, GWA studies reveal common risk SNPs ( 92 , 185 – 188 ). In addition, studies have implicated CD8+ T cells in Hashimoto’s thyroiditis, MS, and Addison’s Disease, similar to vitiligo ( 189 – 192 ), as well as an important role for the IFN-γ chemokine axis during pathogenesis. IFN-γ and CXCL10 are expressed in human islets to recruit lymphocytes in T1D, autoreactive cells produce IFN-γ in Addison’s Disease, and IFN-γ level positively correlates with disease severity in Hashimoto’s thyroiditis ( 193 – 196 ).…”

Section: Using Vitiligo To Understand Organ-specific Autoimmunitymentioning

confidence: 99%

Translational Research in Vitiligo

Katz

Harris

2021

Front. Immunol.

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Vitiligo is a disease of the skin characterized by the appearance of white spots. Significant progress has been made in understanding vitiligo pathogenesis over the past 30 years, but only through perseverance, collaboration, and open-minded discussion. Early hypotheses considered roles for innervation, microvascular anomalies, oxidative stress, defects in melanocyte adhesion, autoimmunity, somatic mosaicism, and genetics. Because theories about pathogenesis drive experimental design, focus, and even therapeutic approach, it is important to consider their impact on our current understanding about vitiligo. Animal models allow researchers to perform mechanistic studies, and the development of improved patient sample collection methods provides a platform for translational studies in vitiligo that can also be applied to understand other autoimmune diseases that are more difficult to study in human samples. Here we discuss the history of vitiligo translational research, recent advances, and their implications for new treatment approaches.

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“…It is characterized by a high level of the thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) in patients' serum, and patients' goiters may have a large amount of lymphocyte infiltration or even form lymphoid follicles (Antonelli et al 2015). The cells infiltrating the thyroid gland are mainly T cells, especially CD4 + T cells, which are directly related to inflammation and thyroid cell destruction (Luty et al 2019). Pro-inflammatory cytokines and the chemokines produced by CD4 + T cells directly lead to thyroid inflammation and recruit more T cells into the thyroid, aggravating the inflammatory response (Li et al 2019b, Luty et al 2019.…”

Section: Introductionmentioning

confidence: 99%

“…The cells infiltrating the thyroid gland are mainly T cells, especially CD4 + T cells, which are directly related to inflammation and thyroid cell destruction (Luty et al 2019). Pro-inflammatory cytokines and the chemokines produced by CD4 + T cells directly lead to thyroid inflammation and recruit more T cells into the thyroid, aggravating the inflammatory response (Li et al 2019b, Luty et al 2019. The destruction of thyroid follicles may lead to hypothyroidism (Antonelli et al 2015).…”

Section: Introductionmentioning

confidence: 99%

LncRNA profile in Hashimoto’s thyroiditis and potential function of NONHSAT079547.2

Luo

Wang

2020

Journal of Molecular Endocrinology

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Hashimoto’s thyroiditis (HT) is a common organ-specific autoimmune disease, which develops in 0.3–1.5/1000 subjects annually. The aims of this study were to determine the lncRNA profile in peripheral blood CD4+ T cells from HT patients and then to characterize the potential function of NONHSAT079547.2. A total of 37 HT patients and 50 sex- and age-matched healthy controls were enrolled for high-throughput sequencing. Another 43 HT patients and 50 sex- and age-matched controls were enrolled for validation via real-time PCR. Flow cytometry and CCK8 assays were used to measure cell apoptosis and growth levels. Western blotting was used for measuring the expression of growth- and apoptosis-associated proteins. IL-17 serum concentration and transcriptional level in CD4+ T cells of participants were detected by ELISA and real-time PCR, respectively. The mechanism of competitive endogenous RNA was determined using real-time PCR, ELISA, RNA immunoprecipitation, and dual-luciferase assays in Jurkat cells. A total of 7564 significantly differentially expressed lncRNAs were found, of which 3913 lncRNAs were upregulated and 3651 lncRNAs were downregulated in HT group when compared to control group. NONHSAT079547.2 was significantly upregulated in HT patients and was positively correlated with serum thyroid peroxidase antibody level. Further studies confirmed that NONHSAT079547.2 could promote cell growth and control IL-17 expression and secretion via the NONHSAT079547.2/miR-4716-5p/IL-17 axis.This is the first study to describe the lncRNA profile in CD4+ T cells of HT patients. The studies on the function of NONHSAT079547.2 might elucidate the underlying molecular mechanisms and represent potential biomarkers for HT.

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Immunological aspects of autoimmune thyroid disease – Complex interplay between cells and cytokines

Cited by 60 publications

References 37 publications

Familial risks between Graves disease and Hashimoto thyroiditis and other autoimmune diseases in the population of Sweden

Familial risks between Graves disease and Hashimoto thyroiditis and other autoimmune diseases in the population of Sweden

Translational Research in Vitiligo

LncRNA profile in Hashimoto’s thyroiditis and potential function of NONHSAT079547.2

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