IL-7Rα and L-selectin, but not CD103 or CD34, are required for murine peanut-induced anaphylaxis
Allergy to peanuts results in severe anaphylactic responses in affected individuals, and has dramatic effects on society and public policy. Despite the health impacts of peanut-induced anaphylaxis (PIA), relatively little is known about immune mechanisms underlying the disease. Using a mouse model of PIA, we evaluated mice with deletions in four distinct immune molecules (IL7Rα, L-selectin, CD34, CD103), for perturbed responses.
PIA was induced by intragastric sensitization with peanut antigen and cholera toxin adjuvant, followed by intraperitoneal challenge with crude peanut extract (CPE). Disease outcome was assessed by monitoring body temperature, clinical symptoms, and serum histamine levels. Resistant mice were evaluated for total and antigen specific serum IgE, as well as susceptibility to passive systemic anaphylaxis.
PIA responses were dramatically reduced in IL7Rα−/− and L-selectin−/− mice, despite normal peanut-specific IgE production and susceptibility to passive systemic anaphylaxis. In contrast, CD34−/− and CD103−/− mice exhibited robust PIA responses, indistinguishable from wild type controls.
Loss of L-selectin or IL7Rα function is sufficient to impair PIA, while CD34 or CD103 ablation has no effect on disease severity. More broadly, our findings suggest that future food allergy interventions should focus on disrupting sensitization to food allergens and limiting antigen-specific late-phase responses. Conversely, therapies targeting immune cell migration following antigen challenge are unlikely to have significant benefits, particularly considering the rapid kinetics of PIA.
- IL-7Rα and L-selectin, but not CD103 or CD34, are required for murine peanut-induced anaphylaxis
- Open Access
- Available under Open Access This content is freely available online to anyone, anywhere at any time.
Allergy, Asthma & Clinical Immunology
- Online Date
- August 2012
- Online ISSN
- BioMed Central
- Additional Links
- Animal model
- Food allergy
- Peanut allergy
- Author Affiliations
- 1. The Biomedical Research Centre, University of British Columbia, Vancouver, BC, Canada
- 2. Department of Microbiology & Immunology, Dalhousie University, Halifax, NS, Canada