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An obligate role for T-cell receptor αβ+ T cells but not T-cell receptor γδ+ T cells, B cells, or CD40/CD40L interactions in a mouse model of atopic dermatitis

Authors :
Raif S. Geha
Emiko Mizoguchi
Amy L. Woodward
Harri Alenius
Scott R. Brodeur
Atul K. Bhan
Jonathan M. Spergel
Hans C. Oettgen
Emanuela Castigli
Source :
Journal of Allergy and Clinical Immunology. 107:359-366
Publication Year :
2001
Publisher :
Elsevier BV, 2001.

Abstract

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 T H 2 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 T H 2 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 α –/– 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 δ –/– mice after sensitization. Absence of CD40 had no effect on these responses. Conclusion: These results suggest that αβ T cells, but not γδ T cells, B cells, or CD40L-CD40 interactions, are critical for skin inflammation and the T H 2 response in AD. (J Allergy Clin Immunol 2001;107:359-66.)

Details

ISSN :
00916749
Volume :
107
Database :
OpenAIRE
Journal :
Journal of Allergy and Clinical Immunology
Accession number :
edsair.doi.dedup.....220a3bb42feaa03f4fc48e5ba8cf5155
Full Text :
https://doi.org/10.1067/mai.2001.112695