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Article: Exogenous type-1 cytokines modulate mercury-induced hyper-IgE in the rat

TitleExogenous type-1 cytokines modulate mercury-induced hyper-IgE in the rat
Authors
Issue Date2000
Citation
Clinical and Experimental Immunology, 2000, v. 121 n. 1, p. 17-22 How to Cite?
AbstractSuppression 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 (HgCl 2) 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-γ) and IL-12. We now report the effects of administration of exogenous type-1 cytokines on HgCl 2- induced Th2 responses. At high doses, recombinant rat IFN-γ markedly reduced serum IgE levels. Recombinant mouse IL-12 was less effective at suppressing the IgE response following HgCl 2, although it caused marked up-regulation of IFN-γ gene expression in the spleen. In Lewis rats, which are resistant to HgCl 2-induced autoimmunity, a rise in serum IFN-γ was observed after HgCl 2, but administration of polyclonal anti-IFN-γ antibodies did not render them susceptible to induction of a Th2 response by HgCl 2. Our data show that individual type-1 cytokines are capable of suppressing the dramatic Th2 response induced by HgCl 2 in the rat, even when they are not given until after starting HgCl 2 administration. IFN-γ 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.
Persistent Identifierhttp://hdl.handle.net/10722/195360
ISSN
2015 Impact Factor: 3.148
2015 SCImago Journal Rankings: 1.369
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGorrie, MJ-
dc.contributor.authorQasim, FJ-
dc.contributor.authorWiiittle, CJ-
dc.contributor.authorGillespie, KM-
dc.contributor.authorSzeto, C-C-
dc.contributor.authorNicoletti, F-
dc.contributor.authorBolton, EM-
dc.contributor.authorBradley, JA-
dc.contributor.authorMathieson, PW-
dc.date.accessioned2014-02-28T06:12:02Z-
dc.date.available2014-02-28T06:12:02Z-
dc.date.issued2000-
dc.identifier.citationClinical and Experimental Immunology, 2000, v. 121 n. 1, p. 17-22-
dc.identifier.issn0009-9104-
dc.identifier.urihttp://hdl.handle.net/10722/195360-
dc.description.abstractSuppression 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 (HgCl 2) 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-γ) and IL-12. We now report the effects of administration of exogenous type-1 cytokines on HgCl 2- induced Th2 responses. At high doses, recombinant rat IFN-γ markedly reduced serum IgE levels. Recombinant mouse IL-12 was less effective at suppressing the IgE response following HgCl 2, although it caused marked up-regulation of IFN-γ gene expression in the spleen. In Lewis rats, which are resistant to HgCl 2-induced autoimmunity, a rise in serum IFN-γ was observed after HgCl 2, but administration of polyclonal anti-IFN-γ antibodies did not render them susceptible to induction of a Th2 response by HgCl 2. Our data show that individual type-1 cytokines are capable of suppressing the dramatic Th2 response induced by HgCl 2 in the rat, even when they are not given until after starting HgCl 2 administration. IFN-γ 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.-
dc.languageeng-
dc.relation.ispartofClinical and Experimental Immunology-
dc.titleExogenous type-1 cytokines modulate mercury-induced hyper-IgE in the rat-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-2249.2000.01261.x-
dc.identifier.pmid10886234-
dc.identifier.scopuseid_2-s2.0-0033934315-
dc.identifier.volume121-
dc.identifier.issue1-
dc.identifier.spage17-
dc.identifier.epage22-
dc.identifier.isiWOS:000087856600004-

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