Enhancement of IgE production by anti-CD40 antibody in atopic dermatitis

Harald Renz, Chaya Brodie, Katherine Bradley, Donald Y.M. Leung, Erwin W. Gelfand

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    19 Scopus citations

    Abstract

    It has been recently recognized that the obligate requirement for T cells in the development of IgE responses can be substituted for by anti-CD40 antibody. In this study of patients with atopic dermatitis and high IgE levels, we have analyzed the role of the CD40 molecule in IgE production. Costimulation of peripheral blood mononuclear cells (PBMCs) from normal donors with interleukin-4 (IL-4) and anti-CD40 monoclonal antibody resulted in a selective increase in IgE production; either reagent alone, however, was ineffective. In contrast, addition of anti-CD40 monoclonal antibody alone to PBMCs or B cells from patients with atopic dermatitis markedly increased IgE production, even in the absence of exogenous IL-4. With the use of an ELISA spot assay, this increase in IgE production was attributed to an expansion of IgE-secreting B cells. In anti-IgM-stimulated lymphocyte cultures from patients with atopic dermatitis the costimulation with anti-CD40 induced strong lymphocyte proliferation. Similar results were observed with anti-IgM plus IL-4. The augmentation induced by anti-CD40 was inhibited by addition of anti-IL4 to anti-CD40-treated atopic dermatitis cells. In normal subjects the effects of anti-CD40 alone on IgE production could be observed after pretreatment of normal PBMCs with IL-4 for 3 days. The effects of anti-CD40 in atopic dermatitis may be explained in part by differences in CD40 expression. In freshly isolated PBMCs from patients with atopic dermatitis, the mean fluorescence intensity of CD40 expression on B cells was increased when compared with PBMCs from nonatopic donors, and stimulation of normal or atopic dermatitis PBMCs with IL-4 increased the intensity of CD40 staining of cells. (J ALLERGY CLIN IMMUNOL 1994;93:658-68.).

    Original languageEnglish
    Pages (from-to)658-668
    Number of pages11
    JournalJournal of Allergy and Clinical Immunology
    Volume93
    Issue number3
    DOIs
    StatePublished - Mar 1994

    Funding

    FundersFunder number
    National Institute of Allergy and Infectious DiseasesR01AI026490

      Keywords

      • B cells
      • CD40
      • IgE
      • atopic dermatitis
      • interleukin-4

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