The role of regulatory T cells and genes involved in their differentiation in pathogenesis of selected inflammatory and neoplastic skin diseases. Part III: Polymorphisms of genes involved in Tregs’ activation and function

Nedoszytko, Bogusław; Sokołowska‐Wojdyło, Małgorzata; Renke, Joanna; Lange, Magdalena; Trzonkowski, Piotr; Sobjanek, Michał; Szczerkowska-Dobosz, Aneta; Niedoszytko, Marek; Górska, Aleksandra; Romantowski, Jan; Skokowski, Jarosław; Nowicki, Roman

doi:10.5114/pdia.2017.67053

Cited by 9 publications

(9 citation statements)

References 113 publications

(88 reference statements)

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“…Environmental factors, genetic defects, and hormones can regulate immune responses and therefore may influence SLE susceptibility (64)(65)(66)(67). Regulatory T cells (T regs ) play a key role in maintaining immune homeostasis including the prevention of autoimmunity, maintenance of self-tolerance, and regulation Genetic polymorphisms in the FoxP3 gene and imbalances of regulatory T cells and autoimmunity have also been reported (86) as-well-as polymorphisms of genes involved in T regs activation and function (87). Gender effects have also been reported.…”

Section: Discussionmentioning

confidence: 99%

“…Regulatory B cells (B reg ) and myeloid-derived suppressor cells (MDSC) ( 74 – 79 ) and type1 regulatory T cells (CD4 + IL-10 + FoxP3 − ) ( 80 – 85 ) have an immunosuppression role and promote immune tolerance. Genetic polymorphisms in the FoxP3 gene and imbalances of regulatory T cells and autoimmunity have also been reported ( 86 ) as-well-as polymorphisms of genes involved in T regs activation and function ( 87 ). Gender effects have also been reported.…”

Section: Discussionmentioning

confidence: 99%

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Sex Hormones and Gender Influence the Expression of Markers of Regulatory T Cells in SLE Patients

Singh

Bischoff

2021

Front. Immunol.

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Regulatory T cells have been implicated in the regulation and maintenance of immune homeostasis. Whether gender and sex hormones differentially influence the expression and function of regulatory T cell phenotype and their influence on FoxP3 expression remains obscure. We provide evidence in this study that the number and percent of human regulatory T cells (Tregs) expressing CD4+ and CD8+ are significantly reduced in healthy females compared to healthy males. In addition, both CD4+CD25+hi and CD8+CD25+hi subsets in healthy males have a 2-3 fold increase in FoxP3 mRNA expression compared to healthy females. Female SLE patients, compared to healthy women, have elevated plasma levels of estradiol and decreased levels of testosterone. Higher levels of testosterone correlate with higher expression of FoxP3 in CD4+CD25hiCD127low putative Tregs in women with SLE. Incubation of CD4+ regulatory T cells with 17β-estradiol at physiological levels generally decreased FoxP3 expression in females with SLE. These data suggest that females may be more susceptible than males to SLE and other autoimmune diseases in part because they have fewer Tregs and reduced FoxP3 expression within those cells due to normal E2 levels which suppress FoxP3 expression. In addition, low levels of plasma testosterone in women may further reduce the ability of the Tregs to express FoxP3. These data suggest that gender and sex hormones can influence susceptibility to SLE via effects on regulatory T cells and FoxP3 expression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Sex Hormones and Gender Influence the Expression of Markers of Regulatory T Cells in SLE Patients

Singh

Bischoff

2021

Front. Immunol.

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“…In AD pathogenesis, the demethylation, acetylation, and methylation of the H3 residue in the FOXP3 promoter gene region, along with the hypermethylation of the RORC gene and the methylation of the H3 residue, promote the regulation of Th0 cells. The differentiation of Tregs, 34 , 92 , 94 , 95 thereby reduce the levels of histone acetylation at Th1 and regulatory sites. 128…”

Section: Mechanismmentioning

confidence: 99%

Pathogenesis of allergic diseases and implications for therapeutic interventions

Wang

Zhou

Zhang

et al. 2023

Sig Transduct Target Ther

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Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. Accompanied by high recurrence rates, the steadily rising incidence rates of these diseases are attracting increasing attention. The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. With the rapid development of immunology, molecular biology, and biotechnology, many new biological drugs have been designed for the treatment of allergic diseases, including anti-immunoglobulin E (IgE), anti-interleukin (IL)-5, and anti-thymic stromal lymphopoietin (TSLP)/IL-4, to control symptoms. For doctors and scientists, it is becoming more and more important to understand the influencing factors, pathogenesis, and treatment progress of allergic diseases. This review aimed to assess the epidemiology, pathogenesis, and therapeutic interventions of allergic diseases, including AR, AAS, AD, and FA. We hope to help doctors and scientists understand allergic diseases systematically.

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“…The demethylation of the region in the FOXP3 promoter gene, H3 residue acetylation, and methylations, accompanied by the hypermethylation of the RORC gene and H3 residue methylations favors the differentiation of the Th0 cells towards regulatory T (Treg) phenotype. In contrast, the methylation of the FOXP3 promoter and the demethylation of RORC results in Treg deficiency, one of the features in AD pathogenesis [43,45,[50][51][52].…”

Section: Methylation Hydroxymethylation or Demethylation Of Cytosinementioning

confidence: 99%

Genetic and Epigenetic Aspects of Atopic Dermatitis

Nedoszytko

Reszka

Gutowska-Owsiak

et al. 2020

IJMS

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Atopic dermatitis is a heterogeneous disease, in which the pathogenesis is associated with mutations in genes encoding epidermal structural proteins, barrier enzymes, and their inhibitors; the role of genes regulating innate and adaptive immune responses and environmental factors inducing the disease is also noted. Recent studies point to the key role of epigenetic changes in the development of the disease. Epigenetic modifications are mainly mediated by DNA methylation, histone acetylation, and the action of specific non-coding RNAs. It has been documented that the profile of epigenetic changes in patients with atopic dermatitis (AD) differs from that observed in healthy people. This applies to the genes affecting the regulation of immune response and inflammatory processes, e.g., both affecting Th1 bias and promoting Th2 responses and the genes of innate immunity, as well as those encoding the structural proteins of the epidermis. Understanding of the epigenetic alterations is therefore pivotal to both create new molecular classifications of atopic dermatitis and to enable the development of personalized treatment strategies.

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The role of regulatory T cells and genes involved in their differentiation in pathogenesis of selected inflammatory and neoplastic skin diseases. Part III: Polymorphisms of genes involved in Tregs’ activation and function

Cited by 9 publications

References 113 publications

Sex Hormones and Gender Influence the Expression of Markers of Regulatory T Cells in SLE Patients

Sex Hormones and Gender Influence the Expression of Markers of Regulatory T Cells in SLE Patients

Pathogenesis of allergic diseases and implications for therapeutic interventions

Genetic and Epigenetic Aspects of Atopic Dermatitis

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