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Increased numbers of FoxP3-expressing CD4+ CD25+ regulatory T cells in peripheral blood from dogs with atopic dermatitis and its correlation with disease severity


Hauck, V; Hügli, P; Meli, M L; Rostaher, A; Fischer, N; Hofmann-Lehmann, R; Favrot, C (2016). Increased numbers of FoxP3-expressing CD4+ CD25+ regulatory T cells in peripheral blood from dogs with atopic dermatitis and its correlation with disease severity. Veterinary Dermatology, 27(1):26-e9.

Abstract

BACKGROUND Atopic dermatitis (AD) is a common chronic inflammatory skin disease of humans and dogs. Regulatory T cells (Tregs) are essential controllers of immune homeostasis and have been shown to play a key role in human AD, even though frequencies of Tregs in atopic human patients vary greatly. Only two studies have reported Treg numbers in the peripheral blood of dogs with canine AD (CAD). OBJECTIVES This study aimed to assess the numbers of circulating Tregs in healthy and atopic dogs, and to determine whether Treg numbers correlate with age, sex, disease severity or pre-treatment. ANIMALS Client-owned dogs including 14 healthy dogs and 35 dogs with CAD. METHODS Expression of Tregs in peripheral blood mononuclear cells was evaluated by flow cytometry. Tregs were phenotypically identified as T cells triple positive for CD4, CD25 and FoxP3. RESULTS The percentage of circulating CD4(+) CD25(+) FoxP3(+) Tregs in atopic dogs was increased significantly compared to healthy dogs (mean 2.1% versus 1%, P = 0.002) and correlated with disease severity (Pruritus Scale: r = 0.48, P = 0.003; CADESI-04: r = 0.34, P = 0.044). No significant differences in age or sex were found in either group and pre-treatment had no influence on results for atopic dogs. CONCLUSIONS Data suggest that, as in humans, CD4(+) CD25(+) FoxP3(+) Tregs may contribute to the pathogenesis of CAD as indicated by an association between Treg frequency and disease severity. Further investigation is required to improve the understanding of the role of Tregs in atopic dogs.

Abstract

BACKGROUND Atopic dermatitis (AD) is a common chronic inflammatory skin disease of humans and dogs. Regulatory T cells (Tregs) are essential controllers of immune homeostasis and have been shown to play a key role in human AD, even though frequencies of Tregs in atopic human patients vary greatly. Only two studies have reported Treg numbers in the peripheral blood of dogs with canine AD (CAD). OBJECTIVES This study aimed to assess the numbers of circulating Tregs in healthy and atopic dogs, and to determine whether Treg numbers correlate with age, sex, disease severity or pre-treatment. ANIMALS Client-owned dogs including 14 healthy dogs and 35 dogs with CAD. METHODS Expression of Tregs in peripheral blood mononuclear cells was evaluated by flow cytometry. Tregs were phenotypically identified as T cells triple positive for CD4, CD25 and FoxP3. RESULTS The percentage of circulating CD4(+) CD25(+) FoxP3(+) Tregs in atopic dogs was increased significantly compared to healthy dogs (mean 2.1% versus 1%, P = 0.002) and correlated with disease severity (Pruritus Scale: r = 0.48, P = 0.003; CADESI-04: r = 0.34, P = 0.044). No significant differences in age or sex were found in either group and pre-treatment had no influence on results for atopic dogs. CONCLUSIONS Data suggest that, as in humans, CD4(+) CD25(+) FoxP3(+) Tregs may contribute to the pathogenesis of CAD as indicated by an association between Treg frequency and disease severity. Further investigation is required to improve the understanding of the role of Tregs in atopic dogs.

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2 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:05 Vetsuisse Faculty > Veterinary Clinic > Department of Farm Animals
05 Vetsuisse Faculty > Veterinary Clinic > Department of Small Animals
Dewey Decimal Classification:570 Life sciences; biology
630 Agriculture
Language:English
Date:February 2016
Deposited On:10 Jun 2016 12:40
Last Modified:11 Jun 2016 08:07
Publisher:Wiley-Blackwell Publishing, Inc.
ISSN:0959-4493
Publisher DOI:https://doi.org/10.1111/vde.12279
PubMed ID:26748886

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