Lack of interleukin-33 and its receptor does not prevent calcipotriol-induced atopic dermatitis-like inflammation in mice

Autor:	Clara Hammarström, Wojciech Pietka, Denis Khnykin, Manuela Zucknick, Olav Sundnes, Guttorm Haraldsen
Jazyk:	angličtina
Rok vydání:	2020
Předmět:	Male CD3 Translational immunology lcsh:Medicine Inflammation Granulocyte Article Dermatitis Atopic chemistry.chemical_compound Mice Calcitriol Medicine Animals Humans Receptor lcsh:Science Calcipotriol Skin Mice Knockout Multidisciplinary biology business.industry Interleukins lcsh:R Atopic dermatitis medicine.disease Interleukin-33 Interleukin-1 Receptor-Like 1 Protein Interleukin 33 Disease Models Animal medicine.anatomical_structure chemistry Immunology biology.protein Female lcsh:Q medicine.symptom business Infiltration (medical) Signal Transduction
Zdroj:	Scientific Reports, Vol 10, Iss 1, Pp 1-8 (2020) Scientific Reports
ISSN:	2045-2322
DOI:	10.1038/s41598-020-63410-z
Popis:	Current studies addressing the influence of interleukin-33 or its receptor (IL-33R/ST2) on development of atopic dermatitis-like inflammation in mice have reported conflicting results. We compared the response in single- and double-deficient IL-33−/−/ST2−/− C57BL/6J BomTac mice in the well-established calcipotriol-induced model of atopic dermatitis. All genotypes (groups of up to 14 mice) developed atopic dermatitis-like inflammation yet we observed no biologically relevant difference between groups in gross anatomy or ear thickness. Moreover, histological examination of skin revealed no differences in mononuclear leukocyte and granulocyte infiltration nor Th2 cytokine levels (IL-4 and IL-13). Finally, skin CD45+ cells and CD3+ cells were found at similar densities across all groups. Our findings indicate that lack of interleukin-33 and its receptor ST2 does not prevent the development of AD-like skin inflammation.
Databáze:	OpenAIRE
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