| Mononuclear cells from patients with the hyper-IgE syndrome produce little IgE when they are stimulated with recombinant human interleukin-4. | |
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MedLine Citation:
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PMID: 1720150 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To investigate whether B cells from patients with the hyper-IgE syndrome are more sensitive to the effects of interleukin-4 in vitro than B cells of normal or atopic individuals, we stimulated blood mononuclear cells (MNC) with varying doses of recombinant human interleukin 4 (rhIL-4) and measured supernatant IgE concentrations after 18 days of culture. Geometric mean spontaneous IgE synthesis after 18 days of culture without rhIL-4 was low (less than 3 ng/ml) and similar for MNCs from nine patients with the hyper-IgE syndrome, nine atopic and nine normal subjects. As found in our previous studies, MNCs from the nine atopic and the nine normal donors produced significant and similar quantities of IgE (geometric mean maximum IgE, 25.2 and 18.7 ng/ml, respectively) when MNCs were stimulated with rhIL-4. MNCs from both donor groups had similar sensitivity to the concentration of IL-4 eliciting the IgE response. In striking contrast, MNCs from the nine patients with the hyper-IgE syndrome failed to produce significant IgE over that produced spontaneously when MNCs were stimulated by a wide range of rhIL-4 concentrations. Coculture of B cell-enriched subpopulations from patients with the hyper-IgE syndrome with T cell-enriched subpopulations from nonatopic and atopic donors failed to restore responsiveness to rhIL-4. The addition of anti-CD40 monoclonal antibody to MNC cultures did result in enhancement of rhIL-4 IgE synthesis by MNCs from patients with the hyper-IgE syndrome, but the concentration of anti-CD40 required to elicit this enhancement was tenfold higher than for control MNCs.(ABSTRACT TRUNCATED AT 250 WORDS) |
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Authors:
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J J Claasen; A D Levine; S E Schiff; R H Buckley |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The Journal of allergy and clinical immunology Volume: 88 ISSN: 0091-6749 ISO Abbreviation: J. Allergy Clin. Immunol. Publication Date: 1991 Nov |
Date Detail:
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Created Date: 1991-12-30 Completed Date: 1991-12-30 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 1275002 Medline TA: J Allergy Clin Immunol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 713-21 Citation Subset: AIM; IM |
Affiliation:
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Department of Pediatrics, Duke University School of Medicine, Durham, N.C. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Antibodies, Monoclonal / immunology Antigens, CD / immunology Antigens, CD40 Antigens, Differentiation, B-Lymphocyte / immunology B-Lymphocytes / immunology Cells, Cultured Child Female Humans Hypersensitivity, Immediate / immunology Immunoglobulin E / analysis, biosynthesis* Interleukin-4 / pharmacology* Job's Syndrome / immunology* Leukocytes, Mononuclear / immunology* Lymphocyte Activation Male Recombinant Proteins / pharmacology T-Lymphocytes / immunology |
| Grant Support | |
ID/Acronym/Agency:
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AI12026/AI/NIAID NIH HHS; AI28414/AI/NIAID NIH HHS; M01-RR-30/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Monoclonal; 0/Antigens, CD; 0/Antigens, CD40; 0/Antigens, Differentiation, B-Lymphocyte; 0/Recombinant Proteins; 207137-56-2/Interleukin-4; 37341-29-0/Immunoglobulin E |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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