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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1990-9-20
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pubmed:abstractText |
Previous reports have demonstrated that injection of rIL-1 alpha into mice abrogates the ability of deaggregated human gamma-globulin (HGG) to induce a state of antigen specific immunologic tolerance in vivo. Our results demonstrate that human rIL-1 beta and a bioactive nonapeptide of human IL-1 beta inhibit the induction of tolerance to HGG suggesting that IL-1 affects tolerance induction through a noninflammatory mechanism of action because the immunoactive nonapeptide possesses only immunomodulatory properties. Further, TNF-alpha but not IL-6, cytokines with many bioactivities in common with IL-1, was found to inhibit the induction of tolerance. Therefore, it appears unlikely that IL-6 plays a role in the pathway by which either IL-1 or TNF-alpha interferes with tolerance induction. Although IL-2, IL-4, and IFN-gamma were incapable of directly affecting the induction of tolerance to HGG, it was determined that IL-4 and IFN-gamma were capable of inhibiting the ability of IL-1 to abrogate tolerance induction. It has been suggested that IL-1 induces the generation of endogenous IL-1 in vivo. Further, it has been demonstrated that IFN-gamma as well as IL-4 inhibits the synthesis of IL-1. Inasmuch as IL-4 and IFN-gamma inhibit the ability of IL-1 to abrogate tolerance induction, it appears that it is the endogenously generated IL-1 that interferes with tolerance induction. It was also determined that neither IL-4 nor IFN-gamma inhibits the activity of IL-1 which is consistent with results reported by others. Thus, results presented here suggest that the inhibition of tolerance induction to HGG by IL-1 may involve the stimulation of endogenous IL-1 synthesis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Biological Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/gamma-Globulins
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
145
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1318-23
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:1696593-Amino Acid Sequence,
pubmed-meshheading:1696593-Animals,
pubmed-meshheading:1696593-Biological Factors,
pubmed-meshheading:1696593-Cytokines,
pubmed-meshheading:1696593-Female,
pubmed-meshheading:1696593-Immune Tolerance,
pubmed-meshheading:1696593-Interferon-gamma,
pubmed-meshheading:1696593-Interleukin-1,
pubmed-meshheading:1696593-Interleukin-4,
pubmed-meshheading:1696593-Interleukin-6,
pubmed-meshheading:1696593-Lymphocyte Activation,
pubmed-meshheading:1696593-Mice,
pubmed-meshheading:1696593-Mice, Inbred CBA,
pubmed-meshheading:1696593-Molecular Sequence Data,
pubmed-meshheading:1696593-Oligopeptides,
pubmed-meshheading:1696593-Recombinant Proteins,
pubmed-meshheading:1696593-Tumor Necrosis Factor-alpha,
pubmed-meshheading:1696593-gamma-Globulins
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pubmed:year |
1990
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pubmed:articleTitle |
The regulatory effects of cytokines on the induction of a peripheral immunologic tolerance in mice.
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pubmed:affiliation |
Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
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