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Article: Role of β1 and β2 subunits of the interleukin-12 receptor in determining T helper 1/T helper 2 responses in vivo in the rat

TitleRole of β1 and β2 subunits of the interleukin-12 receptor in determining T helper 1/T helper 2 responses in vivo in the rat
Authors
Issue Date2000
Citation
Immunology, 2000, v. 99 n. 1, p. 109-112 How to Cite?
AbstractInterleukin-12 (IL-12) responsiveness, and hence capacity to mount a T helper type 1(Th1) immune response, may be regulated via differential expression of the IL-12 receptor β2 subunit at least in vitro in human and murine cells. To test whether a similar phenomenon operates in vivo in the rat we cloned and sequenced partial cDNAs for rat IL-12Rβ1 and IL-12Rβ2 subunits and analysed expression of these genes in vivo in two rat strains with different Th1/Th2 bias. After treatment with mercuric chloride (HgCl2), Brown-Norway rats develop Th2-biased autoimmunity whereas Lewis rats do not develop autoimmunity, instead becoming resistant to Th1-biased diseases to which they are normally susceptible. We report close sequence homology between the segments of the rat IL12R genes sequenced and corresponding mouse genes (95-6% and 92% for IL-12Rβ1 and IL-12Rβ2, respectively). Both Brown-Norway and Lewis rats express both β1 and β2 subunits of IL-12 receptor in vivo in spleen; Brown-Norway rats express the β2 subunit at a lower level than Lewis rats. After HgCl2 treatment, IL-12Rβ1 expression was not altered but there was down-regulation of IL-12Rβ2 expression in both strains. We conclude that relative under-expression of IL-12Rβ2 by Brown-Norway rats contributes to their Th2 bias, and that down-regulation of IL-12Rβ2 after HgCl2 administration in Lewis rats underlies subsequent resistance to induction of Th1-biased diseases.
Persistent Identifierhttp://hdl.handle.net/10722/195358
ISSN
2015 Impact Factor: 4.078
2015 SCImago Journal Rankings: 2.038
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGillespie, KM-
dc.contributor.authorSzeto, C-C-
dc.contributor.authorBetin, VM-
dc.contributor.authorMathieson, PW-
dc.date.accessioned2014-02-28T06:12:02Z-
dc.date.available2014-02-28T06:12:02Z-
dc.date.issued2000-
dc.identifier.citationImmunology, 2000, v. 99 n. 1, p. 109-112-
dc.identifier.issn0019-2805-
dc.identifier.urihttp://hdl.handle.net/10722/195358-
dc.description.abstractInterleukin-12 (IL-12) responsiveness, and hence capacity to mount a T helper type 1(Th1) immune response, may be regulated via differential expression of the IL-12 receptor β2 subunit at least in vitro in human and murine cells. To test whether a similar phenomenon operates in vivo in the rat we cloned and sequenced partial cDNAs for rat IL-12Rβ1 and IL-12Rβ2 subunits and analysed expression of these genes in vivo in two rat strains with different Th1/Th2 bias. After treatment with mercuric chloride (HgCl2), Brown-Norway rats develop Th2-biased autoimmunity whereas Lewis rats do not develop autoimmunity, instead becoming resistant to Th1-biased diseases to which they are normally susceptible. We report close sequence homology between the segments of the rat IL12R genes sequenced and corresponding mouse genes (95-6% and 92% for IL-12Rβ1 and IL-12Rβ2, respectively). Both Brown-Norway and Lewis rats express both β1 and β2 subunits of IL-12 receptor in vivo in spleen; Brown-Norway rats express the β2 subunit at a lower level than Lewis rats. After HgCl2 treatment, IL-12Rβ1 expression was not altered but there was down-regulation of IL-12Rβ2 expression in both strains. We conclude that relative under-expression of IL-12Rβ2 by Brown-Norway rats contributes to their Th2 bias, and that down-regulation of IL-12Rβ2 after HgCl2 administration in Lewis rats underlies subsequent resistance to induction of Th1-biased diseases.-
dc.languageeng-
dc.relation.ispartofImmunology-
dc.titleRole of β1 and β2 subunits of the interleukin-12 receptor in determining T helper 1/T helper 2 responses in vivo in the rat-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-2567.2000.00927.x-
dc.identifier.pmid10651948-
dc.identifier.scopuseid_2-s2.0-0033621675-
dc.identifier.volume99-
dc.identifier.issue1-
dc.identifier.spage109-
dc.identifier.epage112-
dc.identifier.isiWOS:000085240600015-

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