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http://purl.uniprot.org/citations/11174205http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11174205http://www.w3.org/2000/01/rdf-schema#comment"

Background

We recently described a murine model of atopic dermatitis (AD) elicited by epicutaneous sensitization with ovalbumin (OVA). The skin lesions in these mice were characterized by a dermal infiltrate consisting of eosinophils and T cells and by increased expression of the TH2 cytokines IL-4 and IL-5. Epicutaneous sensitization induces a rise in the levels of serum total IgE and OVA-specific antibodies, further indicating that it elicits a predominantly TH2 response.

Objective

This study was undertaken to assess the roles of T cells, B cells, and CD40L-CD40 interactions in AD.

Methods

Mice with targeted gene deletions were sensitized with OVA. Histologic and immunohistochemical examinations, as well as measurements of IL-4 mRNA, were performed on OVA-sensitized skin. Total and antigen-specific serum IgE levels were determined.

Results

RAG2(-/-) mice, which lack both T and B cells, did not exhibit cellular infiltration, induction of dermal IL-4 mRNA, or elevation of serum IgE after OVA sensitization; all of these features were present in B-cell-deficient IgH(-/-) mice. T-cell receptor alpha(-/-) mice did not display cellular infiltration, IL-4 mRNA expression, or increased IgE levels after OVA sensitization, but these responses were elicited in T-cell receptor delta(-/-) mice after sensitization. Absence of CD40 had no effect on these responses.

Conclusion

These results suggest that alphabeta T cells, but not gammadelta T cells, B cells, or CD40L-CD40 interactions, are critical for skin inflammation and the TH2 response in AD."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.org/dc/terms/identifier"doi:10.1067/mai.2001.112695"xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Bhan A.K."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Geha R.S."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Mizoguchi E."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Alenius H."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Spergel J.M."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Oettgen H.C."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Brodeur S.R."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Castigli E."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/author"Woodward A.L."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/name"J Allergy Clin Immunol"xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/pages"359-366"xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/title"An obligate role for T-cell receptor alphabeta+ T cells but not T-cell receptor gammadelta+ T cells, B cells, or CD40/CD40L interactions in a mouse model of atopic dermatitis."xsd:string
http://purl.uniprot.org/citations/11174205http://purl.uniprot.org/core/volume"107"xsd:string
http://purl.uniprot.org/citations/11174205http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11174205
http://purl.uniprot.org/citations/11174205http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11174205
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http://purl.uniprot.org/uniprot/#_A0A075B6A0-mappedCitation-11174205http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11174205
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http://purl.uniprot.org/uniprot/#_P01849-mappedCitation-11174205http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11174205
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