Allergen sensitization stratifies IL-31 production by memory T cells in atopic dermatitis patients.
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PROVIDER: PRJNA938468 | ENA |
REPOSITORIES: ENA
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Project description:The role of allergen sensitization in IL-31 production by T cells and specifically in the clinical context of atopic dermatitis (AD) has not been characterized. The response to house dust mite (HDM) in purified memory T cells cocultured with epidermal cells from AD patients (n=58) and control subjects (n=11) was evaluated. AD-associated cytokines from culture supernatants, plasma proteins and mRNA expression from cutaneous lesions were assessed and related with the clinical features of the patients. HDM-induced IL-31 production by memory T cells defined two subsets of AD patients according to the presence or absence of IL-31 response. Patients in the IL-31 producing group showed a more inflammatory profile, and increased HDM-specific (sp) and total IgE levels compared to the IL-31 non-producing group. A correlation between IL-31 production and patient’s pruritus intensity, plasma CCL27 and periostin was detected. When the same patients were analyzed based on HDM-specific (sp) IgE and total IgE levels, an increased IL-31 in vitro response, as well as type 2 markers in plasma and cutaneous lesions, was found in patients with sp IgE levels > 100 kUA/L and total IgE levels > 1000 kU/L. The IL-31 response by memory T cells was restricted to the cutaneous lymphocyte-associated antigen (CLA)+ T-cell subset. IgE sensitization to HDM allows stratifying IL-31 production by memory T cells in AD patients and relating it to particular clinical phenotypes of the disease.
2023-03-06 | GSE226073 | GEO
Project description:The patho-mechanism of atopic dermatitis showing systemic involvement may be explained by Th17-related cytokines induced by FABP5 through systemic sensitization to a major allergen of a house dust mite.
2020-03-05 | GSE146352 | GEO
Project description:The patho-mechanism of atopic dermatitis showing systemic involvement may be explained by Th17-related cytokines induced by FABP5 through systemic sensitization to a major allergen of a house dust mite.
2020-03-05 | GSE146356 | GEO
Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.
2016-11-13 | GSE72449 | GEO
Project description:BackgroundThe role of allergen sensitization in IL-31 production by T cells and specifically in the clinical context of atopic dermatitis (AD) has not been characterized.MethodsThe response to house dust mite (HDM) in purified memory T cells cocultured with epidermal cells from AD patients (n=58) and control subjects (n=11) was evaluated. AD-associated cytokines from culture supernatants, plasma proteins and mRNA expression from cutaneous lesions were assessed and related with the clinical features of the patients.ResultsHDM-induced IL-31 production by memory T cells defined two subsets of AD patients according to the presence or absence of IL-31 response. Patients in the IL-31 producing group showed a more inflammatory profile, and increased HDM-specific (sp) and total IgE levels compared to the IL-31 non-producing group. A correlation between IL-31 production and patient's pruritus intensity, plasma CCL27 and periostin was detected. When the same patients were analyzed based on sp IgE and total IgE levels, an increased IL-31 in vitro response, as well as type 2 markers in plasma and cutaneous lesions, was found in patients with sp IgE levels > 100 kUA/L and total IgE levels > 1000 kU/L. The IL-31 response by memory T cells was restricted to the cutaneous lymphocyte-associated antigen (CLA)+ T-cell subset.ConclusionIgE sensitization to HDM allows stratifying IL-31 production by memory T cells in AD patients and relating it to particular clinical phenotypes of the disease.
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Project description:The aim of the study was to identify genes which are differentially expressed in the blood of dogs with canine atopic dermatitis (AD) before and after 6 months of allergen-specific immunotherapy (ASIT) in comparison to healthy control dogs. Diagnosis of AD was based on compatible history and clinical signs determined using Willemse and Prélaud diagnostic criteria, completed by Favrot criteria as follows: pruritus sine material, indoor lifestyle and the exclusion of other causes of pruritus ongoing for at least one year. Clinical diagnosis of atopic dermatitis was confirmed by serological allergy testing (IDEXX allergic panel test) and intradermal skin testing (Artuvetrin test set, Netherlands). In order to avoid the role of food antigens as a cause of the skin condition elimination diet was used for 6–8 weeks. No anti-inflammatory drugs were given for at least 3 weeks prior examination with serological test, intradermal test and blood collection. All dogs, which were classified to the investigated group had positive reactions in serological allergy testing and intradermal skin testing. Subsequently, subcutaneous allergen-specific immunotherapy was applied. Allergen extracts were prepared on the basis of the results of intradermal tests by the Artuvetrin company and were administered subcutaneously in increasing concentrations during 6 months according to the manufacturer's recommendations. Aside from gene regulation, this experiment also examined the participation of individual lymphocyte subpopulations (like: B, T, Th, Tc, Treg) and the level of interleukins in the blood of AD dogs before and after therapy.
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Project description:Clinical overlaps between psoriasis and atopic dermatitis are sometimes undiscernible, and there is no consensus whether to treat the overlap phenotype as psoriasis or atopic dermatitis. We enrolled patients diagnosed with either psoriasis or atopic dermatitis, and clinically re-stratified them into classic psoriasis, classic atopic dermatitis, and the overlap phenotype between psoriasis and atopic dermatitis. We compared gene expression profiles of lesional and nonlesional skin biopsy tissues between the three comparison groups. Global mRNA expression and T-cell subset cytokine expression in the skin of the overlap phenotype were consistent with the profiles of psoriasis and different from the profiles of atopic dermatitis. Unsupervised k-means clustering indicated that the best number of distinct clusters for the total population of the three comparison groups was two, and the two clusters of psoriasis and atopic dermatitis were differentiated by gene expression. Our study suggests that clinical overlap phenotype between psoriasis and atopic dermatitis has dominant molecular features of psoriasis, and genomic biomarkers can differentiate psoriasis and atopic dermatitis at molecular levels in patients with a spectrum of psoriasis and atopic dermatitis.
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