Association of functional polymorphisms related to the transcriptional level of <i>FOXP3</i> with prognosis of autoimmune thyroid diseases

Inoue, Naohisa; Watanabe, Mikio; Morita, Mami; Tomizawa, Rina; Akamizu, Takashi; Tatsumi, Ke-ita; Hidaka, Yoh; Iwatani, Yoshinori

doi:10.1111/j.1365-2249.2010.04229.x

Cited by 107 publications

(101 citation statements)

References 17 publications

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“…Wild type AA genotype is 65%, heterozygote AG genotype is 28%, homozygote GG genotype is 4-7% in Asian population. In Caucasion population AA is 60%, AG is 35% and GG is 3-5% [15,27,28]. In our study we found that AA is 63%, AG is 31% and GG is 6% (Table 3).…”

Section: Resultssupporting

confidence: 62%

FOXP3 Promoter polymorphism (-3499 A/G) is not associated with osteoarthritis in a Turkish population

Çekin¹,

Pınarbaşı²,

Dönmez³

et al. 2017

Cumhuriyet Medical Journal

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SUMMARYObjective: In this study we aimed to find out whether FOXP3 promoter region -3499A/G polymorhism was associated with osteoarthiritis in a Turkish population. Method: The study group consists of 50 patients in 3rd stage and 100 patients in 4th stage osteoarthiritis and control group consists of 150 healthy individuals. FOXP3 genotypes were examined by PCR-RFLP method. Results: Our results show that there is no statisticially significant association between osteoarthiritis and FOXP3 -3499A/G polymorphism. The wild type AA genotype was 63%, polymorphic AG was 31% and GG was 6% in the control group, while they were 56%, 37% and 7% in the study group respectively. Conclusions: Osteoarthiritis was seen higher in women than that of men in our study which is compatible with the results of previous results. Keywords: FOXP3, Osteoarthritis, promoter, polymorphism ÖZET Amaç: Bu çalışmada FOXP3 geni promotor bölgesi -3499A/G polimorfizmi ile osteoartrit riski arasındaki ilişki bir Türk popülasyonunda araştırılmıştır. Yöntem: Çalışma grubu, 3. evre 50 ve 4. evre 100 OA hastasından, kontrol grubu ise 150 sağlıklı bireyden oluşmuştur. FOXP3 genotipleri PCR-RFLP yöntemleri kullanılarak elde edilmiştir. Bulgular: Sonuçlarımız istatistiksel olarak OA riski ve FOXP3 geni promotor bölgesi -3499A/G polimorfizmi arasında anlamlı bir ilişki olmadığını göstermiştir. Kontrol grubunda doğal tip AA genotipi %63, polimorfik AG %31 ve GG genotipi oranı % 6 bulunurken çalışma gurubunda bu oranlar sırasıyla %56, %37 ve %7 olarak bulunmuştur. Sonuç: Kadınlarda erkeklere oranla daha sık gözlenmiştir ve bu gözlem, önceki çalışmalarda elde edilen sonuçlar ile uyumludur.

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Section: Resultssupporting

confidence: 62%

FOXP3 Promoter polymorphism (-3499 A/G) is not associated with osteoarthritis in a Turkish population

Çekin¹,

Pınarbaşı²,

Dönmez³

et al. 2017

Cumhuriyet Medical Journal

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“…T-cell depletion enhanced the severity of hyperthyroidism in BALB/c mice immunized with Ad-TSHR289 [24]. A functional single-nucleotide polymorphism (SNP) in the promoter region of Foxp3 was more frequent in patients with GD in remission than in patients with intractable GD [25]. Nakano A [26] has reported an apoptosis-induced decrease in the proportion of intrathyroidal Treg cells in patients with autoimmune thyroid disease.…”

Section: Discussionmentioning

confidence: 98%

Regulatory T cells but not T helper 17 cells are modulated in an animal model of Graves’ hyperthyroidism

Zhou

Fan

et al. 2011

Clin Exp Med

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Graves' disease (GD) involves auto-immunity against thyroid cell antigens, but the reasons for the induction of auto-immunity are uncertain. We wished to investigate the role of T helper 17 (Th17) and regulatory T cells (Treg) in a mouse model of Graves' hyperthyroidism. The model was generated by immunizing mice with adenovirus expressing the autoantigen thyroid-stimulating hormone receptor (Ad-TSHR289). The frequencies of splenic Th17 and Treg were determined by flow cytometry. The levels of interleukin-17(IL-17), forkhead box P3 (Foxp3), and orphan retinoic acid nuclear receptor (RORγt) mRNA were determined by real-time PCR. The number of CD4(+)CD25(+)Foxp3(+) T lymphocyte was significantly reduced in the Ad-TSHR289 group compared with the Ad-control (P < 0.05). mRNA level for Foxp3 was less abundant in Ad-TSHR289 group compared with Ad-control (P < 0.05). However, CD4(+)IL-17(+) T-cell subpopulation and expression of RORγt mRNA did not differ significantly between Ad-TSHR289 and Ad-control groups (P > 0.05). Nevertheless, in Ad-TSHR289 group, a profound increase in the Th17/Treg ratios was found. The present study demonstrates that Th17 is not involved in promoting Graves' hyperthyroidism, while Treg and the ratio of Th17/Treg might play a role in the pathogenesis of Graves' hyperthyroidism.

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“…Several studies have indicated that genetic defects in FOXP3 may lead to its altered levels and functionality and, indeed, autoimmune disorders have been related to various deleterious mutations in FOXP3 [34][35][36][37][38]. With respect to vitiligo, polymorphisms of FOXP3 have been associated with predispostion to the development of the disease (Table 2) [39-41].…”

Section: Forkhead Box P3mentioning

confidence: 99%

Regulatory T cells in vitiligo: Implications for pathogenesis and therapeutics

Dwivedi

Kemp

Laddha

et al. 2015

Autoimmunity Reviews

103

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Vitiligo is a hypomelanotic autoimmune skin disease arising from a breakdown in immunological self-tolerance, which leads to aberrant immune responses against melanocytes.Regulatory T cells (Tregs) are crucial to the development of self-tolerance and so are major foci in the study of autoimmune pathogenesis of vitiligo. This review will summarise recent findings concerning the role of Tregs in the pathogenesis of vitiligo. In addition, as antigen-specific Tregs are a potential route for the reinstatement of immune tolerance, new strategies that expand or induce de novo generation of Tregs and which are currently being investigated as therapies for other autoimmune diseases, will be discussed. These approaches will highlight the opportunities for Treg cell-based therapeutics in vitiligo.4

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Association of functional polymorphisms related to the transcriptional level of FOXP3 with prognosis of autoimmune thyroid diseases

Cited by 107 publications

References 17 publications

FOXP3 Promoter polymorphism (-3499 A/G) is not associated with osteoarthritis in a Turkish population

FOXP3 Promoter polymorphism (-3499 A/G) is not associated with osteoarthritis in a Turkish population

Regulatory T cells but not T helper 17 cells are modulated in an animal model of Graves’ hyperthyroidism

Regulatory T cells in vitiligo: Implications for pathogenesis and therapeutics

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