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Int J Mol Sci. 2023 Dec 28;25(1):404. doi: 10.3390/ijms25010404.
2
Current Insight into the Role of IL-35 and Its Potential Involvement in the Pathogenesis and Therapy of Atopic Dermatitis.当前对 IL-35 作用的深入了解及其在特应性皮炎发病机制和治疗中的潜在作用。
Int J Mol Sci. 2022 Dec 11;23(24):15709. doi: 10.3390/ijms232415709.
3
Pro-Inflammatory versus Anti-Inflammatory cytokines in atopic dermatitis patients: A case control study.特应性皮炎患者的促炎细胞因子与抗炎细胞因子:病例对照研究。
J Cosmet Dermatol. 2022 Nov;21(11):6163-6168. doi: 10.1111/jocd.15182. Epub 2022 Jul 19.
4
The Heterogeneity of Atopic Dermatitis.特应性皮炎的异质性。
J Drugs Dermatol. 2022 Feb 1;21(2):172-176. doi: 10.36849/JDD.6408.
5
Atopic dermatitis: an expanding therapeutic pipeline for a complex disease.特应性皮炎:复杂疾病的治疗领域不断拓展。
Nat Rev Drug Discov. 2022 Jan;21(1):21-40. doi: 10.1038/s41573-021-00266-6. Epub 2021 Aug 20.
6
Subtypes of atopic dermatitis: From phenotype to endotype.特应性皮炎的亚型:从表型到内型。
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7
Which Way Do We Go? Complex Interactions in Atopic Dermatitis Pathogenesis.我们该往何处去?特应性皮炎发病机制中的复杂相互作用。
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8
Genetic and Epigenetic Aspects of Atopic Dermatitis.特应性皮炎的遗传和表观遗传学方面。
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9
Inhibited interleukin 35 expression and interleukin 35-induced regulatory T cells promote type II innate lymphoid cell response in allergic rhinitis.抑制白细胞介素 35 的表达和白细胞介素 35 诱导的调节性 T 细胞促进变应性鼻炎的 II 型先天淋巴细胞反应。
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10
Atopic dermatitis endotypes and implications for targeted therapeutics.特应性皮炎的表型和对靶向治疗的影响。
J Allergy Clin Immunol. 2019 Jan;143(1):1-11. doi: 10.1016/j.jaci.2018.10.032.

白细胞介素-35基因单核苷酸多态性与特应性皮炎之间的关联。

Association between single nucleotide polymorphisms of interleukin-35 genes and atopic dermatitis.

作者信息

Zysk Weronika, Gleń Jolanta, Zabłotna Monika, Nowicki Roman J, Trzeciak Magdalena

机构信息

Department of Dermatology, Venereology and Allergology, Faculty of Medicine, Medical University of Gdansk, Gdansk, Poland.

出版信息

Postepy Dermatol Alergol. 2024 Aug;41(4):415-422. doi: 10.5114/ada.2024.141783. Epub 2024 Jul 25.

DOI:10.5114/ada.2024.141783
PMID:39290904
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11404101/
Abstract

INTRODUCTION

The pathogenesis of atopic dermatitis (AD) involves complex interactions between environmental factors, the skin microbiome, epidermal barrier defects, and altered immune responses that develop on a not fully understood specific genetic background.

AIM

We aimed to evaluate the contribution of single nucleotide polymorphisms (SNPs) in the IL-35 genes ( and ) towards AD susceptibility and clinical characteristics of AD in the Polish population. Two SNPs (rs568408, rs582054) in and one SNP (rs428253) in were selected.

MATERIAL AND METHODS

Blood samples were collected from 202 AD patients and 178 healthy individuals. SNPs in IL-35 genes were analysed by the polymerase chain reaction with sequence-specific primers (SSP-PCR) method.

RESULTS

For rs568408, the AA genotype was significantly linked to increased odds of AD (OR = 34.61; 95% CI: 2.06-579.97, = 0.0137) and marginally associated with normal total serum IgE levels (OR = 2.82; 95% CI: 0.97-8.16; = 0.05), while the GA genotype showed significantly reduced odds of AD (OR = 0.53; 95% CI: 0.34-0.81; = 0.0035). In the context of rs582054, TT genotype carriers had increased odds of AD (OR = 2.05; 95% CI: 1.08-3.85; = 0.03). Patients with the GG genotype of rs428253 had decreased odds of high total serum IgE levels (OR = 0.42; 95% CI: 0.20-0.86; = 0.02) and milder pruritus severity compared to CC genotype carriers (4.12 vs. 7.50; = 0.02).

CONCLUSIONS

IL-35 genetic variations appear to play a role in AD pathogenesis.

摘要

引言

特应性皮炎(AD)的发病机制涉及环境因素、皮肤微生物群、表皮屏障缺陷以及在尚未完全了解的特定遗传背景下发生改变的免疫反应之间的复杂相互作用。

目的

我们旨在评估白细胞介素-35(IL-35)基因(和)中的单核苷酸多态性(SNP)对波兰人群中AD易感性和AD临床特征的影响。在基因中选择了两个SNP(rs568408、rs582054),在基因中选择了一个SNP(rs428253)。

材料与方法

采集了202例AD患者和178名健康个体的血样。采用序列特异性引物聚合酶链反应(SSP-PCR)方法分析IL-35基因中的SNP。

结果

对于基因的rs568408,AA基因型与AD发病几率增加显著相关(OR = 34.61;95%可信区间:2.06 - 579.97,P = 0.0137),并且与正常总血清IgE水平轻度相关(OR = 2.82;95%可信区间:0.97 - 8.16;P = 0.05),而GA基因型显示AD发病几率显著降低(OR = 0.53;95%可信区间:0.34 - 0.81;P = 0.0035)。就基因的rs582054而言,TT基因型携带者AD发病几率增加(OR = 2.05;95%可信区间:1.08 - 3.85;P = 0.03)。与CC基因型携带者相比,基因rs428253的GG基因型患者总血清IgE水平高的几率降低(OR = 0.42;95%可信区间:0.20 - 0.86;P = 0.02),瘙痒严重程度较轻(4.

12对7.50;P = 0.02)。

结论

IL-35基因变异似乎在AD发病机制中起作用。