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Article: Nitric oxide regulates Th1 cell development through the inhibition of IL-12 synthesis by macrophages

TitleNitric oxide regulates Th1 cell development through the inhibition of IL-12 synthesis by macrophages
Authors
KeywordsLeishmania
IL-12
Th1/Th2 cell
Nitric oxide
Macrophage
Issue Date1998
Citation
European Journal of Immunology, 1998, v. 28, n. 12, p. 4062-4070 How to Cite?
AbstractWe have previously reported that mice lacking inducible nitric oxide synthase (NOS2) developed enhanced Th1 cell responses. We now investigated the mechanism by which NO modulates Th1 cells differentiation. Peritoneal macrophages from NOS2-deficient mice infected with Leishmania major in vivo or stimulated with IFN-γ or lipopolysaccharide (LPS) in vitro produced significantly higher levels of IL-12 than those from heterozygous or wild-type mice. A macrophage cell line, J774, produced significant amounts of IL-12 following activation with LPS, or LPS plus IFN-γ. This could be markedly enhanced by the NOS inhibitor L-N(G) monomethyl arginine (L-NMMA), but profoundly inhibited by the NO-generating compound S-nitroso-N-acetyl-penicillamine (SNAP). The effect of NO in this system is selective, since SNAP enhanced and L-NMMA decreased TNF-α synthesis by LPS-activated J774 cells. The differential effect of NO on IL-12 and TNF-α is at the transcriptional level and is activation dependent. Since IL-12 is a major inducer of Th1 cells which produce IFN-γ that can activate macrophages to produce IL-12, our data demonstrate that NO can be an inhibitor of this feedback loop, preventing the excessive amplification of Th1 cells which are implicated in a range of immunopathologies.
Persistent Identifierhttp://hdl.handle.net/10722/200064
ISSN
2015 Impact Factor: 4.179
2015 SCImago Journal Rankings: 2.568
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHuang, Fangping-
dc.contributor.authorNiedbała, Wanda G.-
dc.contributor.authorWei, Xiaoqing-
dc.contributor.authorXu, Damo-
dc.contributor.authorFeng, Guijie-
dc.contributor.authorRobinson, John H.-
dc.contributor.authorLam, Charles-
dc.contributor.authorLiew, Fooyew-
dc.date.accessioned2014-07-26T23:11:05Z-
dc.date.available2014-07-26T23:11:05Z-
dc.date.issued1998-
dc.identifier.citationEuropean Journal of Immunology, 1998, v. 28, n. 12, p. 4062-4070-
dc.identifier.issn0014-2980-
dc.identifier.urihttp://hdl.handle.net/10722/200064-
dc.description.abstractWe have previously reported that mice lacking inducible nitric oxide synthase (NOS2) developed enhanced Th1 cell responses. We now investigated the mechanism by which NO modulates Th1 cells differentiation. Peritoneal macrophages from NOS2-deficient mice infected with Leishmania major in vivo or stimulated with IFN-γ or lipopolysaccharide (LPS) in vitro produced significantly higher levels of IL-12 than those from heterozygous or wild-type mice. A macrophage cell line, J774, produced significant amounts of IL-12 following activation with LPS, or LPS plus IFN-γ. This could be markedly enhanced by the NOS inhibitor L-N(G) monomethyl arginine (L-NMMA), but profoundly inhibited by the NO-generating compound S-nitroso-N-acetyl-penicillamine (SNAP). The effect of NO in this system is selective, since SNAP enhanced and L-NMMA decreased TNF-α synthesis by LPS-activated J774 cells. The differential effect of NO on IL-12 and TNF-α is at the transcriptional level and is activation dependent. Since IL-12 is a major inducer of Th1 cells which produce IFN-γ that can activate macrophages to produce IL-12, our data demonstrate that NO can be an inhibitor of this feedback loop, preventing the excessive amplification of Th1 cells which are implicated in a range of immunopathologies.-
dc.languageeng-
dc.relation.ispartofEuropean Journal of Immunology-
dc.subjectLeishmania-
dc.subjectIL-12-
dc.subjectTh1/Th2 cell-
dc.subjectNitric oxide-
dc.subjectMacrophage-
dc.titleNitric oxide regulates Th1 cell development through the inhibition of IL-12 synthesis by macrophages-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/(SICI)1521-4141(199812)28:12<4062::AID-IMMU4062>3.0.CO;2-K-
dc.identifier.pmid9862342-
dc.identifier.scopuseid_2-s2.0-0031795118-
dc.identifier.volume28-
dc.identifier.issue12-
dc.identifier.spage4062-
dc.identifier.epage4070-
dc.identifier.isiWOS:000077542500017-

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