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2.  IL-7Rα and L-selectin, but not CD103 or CD34, are required for murine peanut-induced anaphylaxis 
Background
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.
Methods
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.
Results
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.
Conclusions
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.
doi:10.1186/1710-1492-8-15
PMCID: PMC3490721  PMID: 22935073
Anaphylaxis; Animal model; Food allergy; Immunity; Peanut allergy
6.  Stem cells, inflammation and allergy 
Recently, many studies have suggested a potential role for early hematopoietic progenitor cell and hematopoietic stem cell (HSC) recruitment and differentiation in the development of allergy and inflammation. This is based largely on evidence that stem cells or CD34+ progenitor cells are recruited to the site of inflammation in allergic diseases, likely through many of the same adhesion and chemokine receptors used for stem cell homing to the bone marrow (PSGL-1, CXCL12, alpha4-beta1 integrin, CD44, etc). Once at the site of inflammation, it has been suggested that stem cells could participate in the perpetuation of inflammation by maturing, locally, into inflammatory cells in response to the growth factors released in situ. Here we provide a brief review of the evidence to suggest that hematopoietic stem and progenitor cells (versus mature hematopoietic lineages) are, indeed, recruited to the site of allergic inflammation. We also discuss the molecules that likely play a role in this process, and highlight a number of our novel observations on a specific role for the stem cell antigen CD34 in this process.
doi:10.1186/1710-1492-5-13
PMCID: PMC2804275  PMID: 20066174

Results 1-6 (6)