Source:http://linkedlifedata.com/resource/pubmed/id/10580421
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
1999-12-13
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pubmed:abstractText |
We evaluated the effects of recombinant human (rh) interleukin (IL)-11 on the development of spontaneous and cyclophosphamide-induced diabetes in female NOD mice. Prolonged treatment with rhIL-11 10 microg i.p. five consecutive times a week between the 4th and 22nd weeks of age significantly suppressed both development and cumulative incidence of type 1 diabetes. Disease protection was transient because most of the animals developed type 1 diabetes within 3 months of treatment withdrawal. In contrast, rhIL-11 failed to prevent type 1 diabetes when administered for the first time to euglycemic 18-week-old NOD mice. Most likely, this discrepancy was not due to age-dependent differences in the immunological responses of NOD mice to rhIL-11 because staphylococcus aureus enterotoxin B-induced tumor necrosis factor (TNF) and IL-12 production were equally suppressed by rhIL-11 in 12- and 25-week-old NOD mice. Relative to controls, NOD mice pretreated with rhIL-11 also showed significantly diminished blood levels of TNF, interferon-gamma, and IL-12 induced by anti-CD3 antibody and/or lipopolysaccharide. The results demonstrate that rhIL-11 has powerful anti-inflammatory effects that are capable of down-regulating early immunodiabetogenic pathways in NOD mice.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclophosphamide,
http://linkedlifedata.com/resource/pubmed/chemical/Enterotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-11,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/enterotoxin B, staphylococcal
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0012-1797
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
48
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2333-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10580421-Aging,
pubmed-meshheading:10580421-Animals,
pubmed-meshheading:10580421-Blood Glucose,
pubmed-meshheading:10580421-Cyclophosphamide,
pubmed-meshheading:10580421-Diabetes Mellitus, Type 1,
pubmed-meshheading:10580421-Enterotoxins,
pubmed-meshheading:10580421-Female,
pubmed-meshheading:10580421-Humans,
pubmed-meshheading:10580421-Interleukin-11,
pubmed-meshheading:10580421-Interleukin-12,
pubmed-meshheading:10580421-Male,
pubmed-meshheading:10580421-Mice,
pubmed-meshheading:10580421-Mice, Inbred NOD,
pubmed-meshheading:10580421-Recombinant Proteins,
pubmed-meshheading:10580421-Time Factors,
pubmed-meshheading:10580421-Tumor Necrosis Factor-alpha
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pubmed:year |
1999
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pubmed:articleTitle |
Early prophylaxis with recombinant human interleukin-11 prevents spontaneous diabetes in NOD mice.
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pubmed:affiliation |
Institute of Microbiology, University of Milan, Italy. ferdinic@ctonline.it
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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