Abstract:
:IL-1 and TNF alpha are assumed to be major mediators of islet cell destruction during the pathogenesis of type 1 diabetes. Here we show by neutralization of the two cytokines with excess antibody that IL-1 and TNF alpha do not contribute to the cytotoxic activity of activated macrophages towards isolated islet cells. However, islet cells can be protected from lysis by depleting the culture medium of L-arginine or by adding the antagonist NG-monomethyl-L-arginine, both of which inhibit the generation of nitric oxide by activated macrophages. These results indicate a role of nitric oxide or its equivalent, the endothelium-derived relaxing factor in the development of type 1 diabetes. This is the first report showing that nitric oxide may damage normal cells and thus may be a hitherto unrecognized pathogenetic factor in tissue inflammation and autoimmune disence.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Kröncke KD,Kolb-Bachofen V,Berschick B,Burkart V,Kolb Hdoi
10.1016/0006-291x(91)91630-usubject
Has Abstractpub_date
1991-03-29 00:00:00pages
752-8issue
3eissn
0006-291Xissn
1090-2104pii
0006-291X(91)91630-Ujournal_volume
175pub_type
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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更新日期:2006-04-21 00:00:00
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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更新日期:2005-09-30 00:00:00