| pubmed-article:10886234 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10886234 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:10886234 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:10886234 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
| pubmed-article:10886234 | lifeskim:mentions | umls-concept:C0205228 | lld:lifeskim |
| pubmed-article:10886234 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:10886234 | pubmed:dateCreated | 2000-8-9 | lld:pubmed |
| pubmed-article:10886234 | pubmed:abstractText | Suppression of IgE responses is a major goal for immunotherapy, especially in the field of allergy. The Th2 subset of helper T cells plays a vital role in class switching of B cells to IgE production by releasing IL-4. In susceptible rat strains, mercuric chloride (HgCl2) induces activation of Th2 cells, with enhanced expression of IL-4, polyclonal B cell activation and very high levels of circulating IgE. We have previously shown that spontaneous regulation of this response coincides with enhanced expression of Th1/type-1 cytokines, including interferon-gamma (IFN-gamma) and IL-12. We now report the effects of administration of exogenous type-1 cytokines on HgCl2-induced Th2 responses. At high doses, recombinant rat IFN-gamma markedly reduced serum IgE levels. Recombinant mouse IL-12 was less effective at suppressing the IgE response following HgCl2, although it caused marked up-regulation of IFN-gamma gene expression in the spleen. In Lewis rats, which are resistant to HgCl2-induced autoimmunity, a rise in serum IFN-gamma was observed after HgCl2, but administration of polyclonal anti-IFN-gamma antibodies did not render them susceptible to induction of a Th2 response by HgCl2. Our data show that individual type-1 cytokines are capable of suppressing the dramatic Th2 response induced by HgCl2 in the rat, even when they are not given until after starting HgCl2 administration. IFN-gamma is a pivotal cytokine in ameliorating the Th2 response and measures aimed at selective up-regulation of this cytokine may be of therapeutic value in suppression of unwanted IgE responses. | lld:pubmed |
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| pubmed-article:10886234 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10886234 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10886234 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10886234 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10886234 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10886234 | pubmed:issn | 0009-9104 | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:NicolettiFF | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:BradleyJ AJA | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:MathiesonP... | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:BoltonE MEM | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:WhittleC JCJ | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:QasimF JFJ | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:GillespieK... | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:SzetoC CCC | lld:pubmed |
| pubmed-article:10886234 | pubmed:author | pubmed-author:GorrieM JMJ | lld:pubmed |
| pubmed-article:10886234 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10886234 | pubmed:volume | 121 | lld:pubmed |
| pubmed-article:10886234 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10886234 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10886234 | pubmed:pagination | 17-22 | lld:pubmed |
| pubmed-article:10886234 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:10886234 | pubmed:meshHeading | pubmed-meshheading:10886234... | lld:pubmed |
| pubmed-article:10886234 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10886234 | pubmed:articleTitle | Exogenous type-1 cytokines modulate mercury-induced hyper-IgE in the rat. | lld:pubmed |
| pubmed-article:10886234 | pubmed:affiliation | Department of Renal Medicine, Western Infirmary, Glasgow, Department of Medicine, University of Cambridge, Cambridge and Academic Renal Unit, University of Bristol, Bristol, UK. | lld:pubmed |
| pubmed-article:10886234 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10886234 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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