Association of polymorphisms in the toll-like receptor genes with atopic dermatitis in the Republic of Bashkortostan

Гималова, Г. Ф.; Карунас, А. С.; Fedorova, Yuliya; Gumennaya , Elvira R.; Levashova, S. V.; Хисматуллина, З. Р.; Prans, Ele; Kõks, Sulev; Эткина, Э. И.; Хуснутдинова, Э. К.

doi:10.1134/s002689331402006x

Cited by 2 publications

(3 citation statements)

References 39 publications

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“…These include toll-like receptors (TLR), proteins containing a nucleotide-binding oligomerization domain (NOD-like receptors or NLRs), a retinoic acid-induced gene, C-type lectin receptors (CLRs), and peptidoglycan recognition proteins (PGRPs). It has been noted that TLR polymorphisms such as TLR1 (rs5743571 and rs5743604), TLR6 (rs5743794) and TLR10 (rs11466617) and genetic variants TLR2 mutations may increase the susceptibility to AD by increasing colonization with Staphylococcus aureus [ 45 , 46 ]. Also, the relationship between R753Q in the TLR2 gene and severe AD is described [ 47 ].…”

Section: Immunological Factorsmentioning

confidence: 99%

Molecular Mechanisms of Atopic Dermatitis Pathogenesis

Sroka-Tomaszewska

Trzeciak

2021

IJMS

226

133

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Atopic dermatitis is a chronic, non-infectious inflammatory dermatosis. Acharacteristic feature is persistent itching of the skin. The chronic, relapsing course of the disease, economic burden, and the whole family’s involvement in the treatment process immensely reduce the quality of life of patients and their families. The disease emerges as a social problem by increasing indirect costs, such as visiting a doctor, absenteeism from work and school, and avoiding social interactions. Thepathophysiology of atopic dermatitis is complex and multifactorial. It includes genetic disorders, a defect in the epidermal barrier, an altered immune response, anddisruption of the skin’s microbial balance. The numerous complex changes at thegenetic level and innate and adaptive immunity provide the basis for characterizing the various phenotypes and endotypes of atopic dermatitis. Emerging therapies rely on the action of specific molecules involved in the disease’s pathogenesis. It may be the starting point for the individualization of atopic dermatitis treatment. This paper will try to present some molecular mechanisms of atopic dermatitis and their clinical implications.

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Section: Immunological Factorsmentioning

confidence: 99%

Molecular Mechanisms of Atopic Dermatitis Pathogenesis

Sroka-Tomaszewska

Trzeciak

2021

IJMS

226

133

View full text Add to dashboard Cite

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“…The first group includes genes, mutations in which lead to the epidermal barrier dysfunction [7,8,[11][12][13]16,[23][24][25]. The second and third groups contain genes associated with the impairment of innate or adaptive immune response mechanisms, respectively, e.g., leading to the over-reactivity in the TLR system, the overproduction of Th2 cytokines or dysfunction in regulatory T lymphocytes; genes encoding Th1, Th17, and Th22 cytokines play essential roles in the chronic phase of the disease [1,7,8,[13][14][15][26][27][28][29][30][31][32].…”

Section: Genetics Of Admentioning

confidence: 99%

“…Table 1. Main groups of genes associated with atopic dermatitis (AD) pathogenesis [5][6][7]9,10,12,[23][24][25][26][27][28][29][30][31][32].…”

Section: Genetics Of Admentioning

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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Association of polymorphisms in the toll-like receptor genes with atopic dermatitis in the Republic of Bashkortostan

Cited by 2 publications

References 39 publications

Molecular Mechanisms of Atopic Dermatitis Pathogenesis

Molecular Mechanisms of Atopic Dermatitis Pathogenesis

Genetic and Epigenetic Aspects of Atopic Dermatitis

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