NDLI: Filaggrin-deficient mice exhibit TH17-dominated skin inflammation and permissiveness to epicutaneous sensitization with protein antigen.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Oyoshi, Michiko K. Murphy, George F. Geha, Raif S.
Description	Country affiliation: United States Author Affiliation: Oyoshi MK ( Division of Immunology, Department of Pediatrics, Harvard Medical School, Children's Hospital, Boston, Mass 02115, USA.)
Abstract	BACKGROUND: Filaggrin is important for skin barrier function and is mutated in 15% to 20% of patients with atopic dermatitis. OBJECTIVE: To examine whether filaggrin deficiency predisposes to skin inflammation and epicutaneous sensitization with protein antigen. METHODS: Skin histology in filaggrin-deficient flaky tail (ft)/ft mice and wild-type controls was assessed by Hematoxylin and Eosin (H&E) staining and immunohistochemistry. Cytokine mRNA expression was examined by quantitative RT-PCR. Serum antibody levels and splenocyte secretion of cytokines were measured by ELISA. RESULTS: The ft/ft mice developed eczematous skin lesions after age 28 weeks and a progressive increase in serum IgE and IgG(1) levels. Normal-appearing skin from 8-week-old ft/ft mice had epidermal thickening and increased dermal infiltration with CD4(+) cells and expression of mRNA for IL-17, IL-6, and IL-23, but not IL-4, IL-13, or IFN-gamma. Lesional skin of 32-week-old ft/ft mice exhibited qualitatively similar, but more pronounced, changes, and elevated IL-4 mRNA levels. Epicutaneous application of ovalbumin to shaved skin of 8-week-old ft/ft mice, but not WT mice, resulted in increased epidermal thickening, dermal infiltration by CD4(+) cells but not eosinophils, and expression of IL-17, IL-6, IL-23, IL-4, and IFN-gamma, but not IL-5 or IL-13, mRNA. Splenocytes from epicutaneously sensitized ft/ft mice, but not controls, secreted cytokines in response to ovalbumin stimulation, and their sera, but not those of controls, contained ovalbumin-specific IgE and IgG(1) antibodies. CONCLUSION: Filaggrin-deficient mice exhibit T(H)17-dominated skin inflammation and eczematous changes with age, and are permissive to epicutaneous sensitization with protein antigen.
File Format	HTM / HTML
ISSN	00916749
e-ISSN	10976825
DOI	10.1016/j.jaci.2009.05.042
Journal	Journal of Allergy and Clinical Immunology
Issue Number	3
Volume Number	124
Language	English
Publisher	Elsevier
Publisher Date	2009-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Immunology Dermatitis, Atopic Immunology Intermediate Filament Proteins Skin T-lymphocytes, Helper-inducer Allergens Animals Cytokines Metabolism Pathology Immunoglobulin E Blood Immunoglobulin G Deficiency Mice Mice, Inbred Balb C Mice, Inbred C57bl Ovalbumin Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Filaggrin deficient mice exhibit Th17-dominated skin inflammation and permissiveness to epicutaneous sensitization with protein antigen

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