Enteric reovirus infection stimulates peanut-specific IgG2a responses in a mouse food allergy model.

Autor: Fecek RJ; Department of Microbiology, Immunology, and Cell Biology, Robert C. Byrd Health Sciences Center of West Virginia University, Morgantown, P.O. Box 9177, WV 26506, USA., Marcondes Rezende M, Busch R, Hassing I, Pieters R, Cuff CF
Jazyk: angličtina
Zdroj: Immunobiology [Immunobiology] 2010 Dec; Vol. 215 (12), pp. 941-8. Date of Electronic Publication: 2010 Mar 04.
DOI: 10.1016/j.imbio.2010.02.004
Abstrakt: IgE-mediated food allergies are an important cause of life-threatening hypersensitivity reactions. Orally administered peanut antigens mixed with the mucosal adjuvant cholera toxin (CT) induce a strong peanut extract (PE)-specific serum IgE response that is correlated with T-helper type 1 (Th1) and type 2 (Th2)-like T-cell responses. This study was conducted to determine if respiratory enteric orphan virus (reovirus), a non-pathogenic virus that induces robust Th1-mediated mucosal and systemic responses could modulate induction of PE-specific allergic responses when co-administered with PE. Young mice were orally exposed to PE mixed with CT, reovirus, or both CT and reovirus. As expected, CT promoted PE-specific serum IgE, IgG1, and IgG2a and intestinal IgA production as well as splenic Th1- and Th2-associated cytokine recall responses. Reovirus did not alter PE-specific serum IgE and IgG1 levels, but substantially increased the PE-specific IgG2a response when co-administered with PE with or without CT. Additionally, reovirus significantly decreased the percentage of the Peyer's patch CD8+ T-cells and Foxp3+CD4+ T-regulatory cells when co-administered with PE. These results demonstrate that an acute mucosal reovirus infection and subsequent Th1 immune response is capable of modulating the Th1/Th2 controlled humoral response to PE. The reovirus-mediated increase in the PE-specific IgG2a antibody response may have therapeutic implications as increased levels of non-allergenic PE-specific IgG2a could block PE antigens from binding to IgE-sensitized mast cells.
(Copyright © 2010 Elsevier GmbH. All rights reserved.)
Databáze: MEDLINE
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