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Upregulation of B7.2, but not B7.1, on B cells from patients with allergic asthma.

Authors: Hofer, MF  Jirapongsananuruk, O  Trumble, AE  Leung, DY 
Citation: Hofer MF, etal., J Allergy Clin Immunol. 1998 Jan;101(1 Pt 1):96-102.
Pubmed: (View Article at PubMed) PMID:9449507
DOI: Full-text: DOI:10.1016/S0091-6749(98)70199-X

BACKGROUND: Allergic asthma is associated with TH2-like cell responses and increased IgE production. Recent studies in mice have suggested that the costimulatory molecule B7.2 (CD86) may influence the development of TH2 cells. OBJECTIVE: We sought to determine the potential role of B7.2 in patients with asthma. METHODS: We performed an analysis of B cells from patients with allergic asthma and healthy control subjects for expression of B7.1 and B7.2 on B cells using five-parameter flow cytometry. RESULTS: We report that atopic patients with asthma who are exposed to allergens have significantly (p < 0.005) higher levels of B7.2 expression on B cells than atopic asthmatic subjects not exposed to allergen in vivo or nonatopic control subjects. In contrast, there were no differences in B7.1 (CD80) expression among the three study subject groups. When peripheral blood mononuclear cells from asthmatic patients or normal control subjects were stimulated with IL-4 or IL-13, the expression of B7.2, but not B7.1, was significantly increased (p < 0.005) on B cells. Interferon-gamma or IL-12 did not affect the expression of either molecule. The functional significance of B7.2 induction by IL-4 in allergic disease was suggested by the increased expression of this molecule on CD23+, but not CD23-, B cells. CONCLUSION: These results indicate that the same B cell involved in allergen presentation also expresses the costimulatory molecule B7.2 and support the hypothesis that this molecule is an important costimulatory molecule in allergic responses, the expression of which can be modulated by TH2-like cytokines.


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CRRD Object Information
CRRD ID: 4892555
Created: 2011-02-23
Species: All species
Last Modified: 2011-02-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.