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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
1994-3-30
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pubmed:abstractText |
We studied the role of IL-4 in human IgE formation in severe combined immunodeficient mice engrafted with peripheral blood mononuclear leukocytes (hu-PBL-SCID). PBL from four nonatopic donors produced only small (< 20 ng/ml) or undetectable amounts of IgE in SCID mice whereas engrafted PBL from seven atopic donors secreted IgE with IgE serum levels reaching a mean +/- SE of 184 +/- 37 ng/ml (n = 20). Serum IgE levels peaked 2-3 wk after PBL transfer and declined thereafter with a half-life of 1-2 wk. In contrast, IgG of all subclasses reached maximum serum levels 5-7 wk after PBL transfer and declined little thereafter. Injection of a neutralizing monoclonal antibody to the human IL-4 receptor (IL-4R) on day 0 inhibited completely the IgE formation and caused an approximate twofold reduction of IgG production of all subclasses. The anti-IL-4 R antibody had no effect on IgE secretion when administered 4 wk after PBL engraftment. Incubation of PBL with IL-4 before engraftment resulted in a 10-fold increase in IgE production and could be further enhanced by 100 fold if, in addition to preincubation with IL-4, IL-4 was injected daily for 5 d after PBL transfer. This treatment with IL-4 also induced two- to threefold increase in IgG levels. IFN-gamma had no effect on either IgE or IgG subclass production. In approximately 50% of the mice, one or more IgG subclasses increased disproportionally 5 wk after PBL injection as a result of monoclonal IgG formation. These data demonstrate that PBL from atopic donors secrete IgE in SCID mice in an IL-4-dependent manner, and that IgE production can be enhanced 10- to 100-fold with exogenous human IL-4 in these mice. This mouse model is amenable for the in vivo study of immunomodulators on human IgE formation.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1312475,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1332484,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1398925,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1401915,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1635839,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1666627,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1731222,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1733515,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1737926,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1890258,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1976649,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1991850,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-1997653,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2060583,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2070573,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2107992,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2109531,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2110199,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2126556,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2388039,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2788092,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2934482,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2970594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-2970644,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-3280724,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-4176112,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-5415911,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-6823332,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-6965297,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113405-8499634
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0021-9738
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
93
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
711-7
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8113405-Animals,
pubmed-meshheading:8113405-Antibodies, Monoclonal,
pubmed-meshheading:8113405-Antibody Formation,
pubmed-meshheading:8113405-Dermatitis, Atopic,
pubmed-meshheading:8113405-Humans,
pubmed-meshheading:8113405-Immunoglobulin E,
pubmed-meshheading:8113405-Immunoglobulin G,
pubmed-meshheading:8113405-Interleukin-4,
pubmed-meshheading:8113405-Lymphocyte Transfusion,
pubmed-meshheading:8113405-Lymphocytes,
pubmed-meshheading:8113405-Mice,
pubmed-meshheading:8113405-Mice, SCID,
pubmed-meshheading:8113405-Receptors, Interleukin-4,
pubmed-meshheading:8113405-Receptors, Mitogen,
pubmed-meshheading:8113405-Time Factors,
pubmed-meshheading:8113405-Transplantation, Heterologous
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pubmed:year |
1994
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pubmed:articleTitle |
Role of interleukin-4 in human immunoglobulin E formation in hu-PBL-SCID mice.
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pubmed:affiliation |
Department of Pediatrics, University of California at San Diego 92093.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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