ArticleDiabetologia1994
Cyclophosphamide treatment of female non-obese diabetic mice causes enhanced expression of inducible nitric oxide synthase and interferon-gamma, but not of interleukin-4.
Article in Diabetologia, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 109 citations in OpenAlex.
- The ratio of serum n-3 to n-6 polyunsaturated fatty acids is associated with diabetes mellitus in patients with prior myocardial infarction: a multicenter cross-sectional study.BMC cardiovascular disorders · 2017Observational
- Histopathological changes in insulin, glucagon and somatostatin cells in the islets of NOD mice during cyclophosphamide-accelerated diabetes: a combined immunohistochemical and histochemical study.Journal of molecular histology · 2005Article
- Role for activating transcription factor 3 in stress-induced beta-cell apoptosis.Molecular and cellular biology · 2004Article
- T-cell reactivity to beta-cell antigens in human insulin-dependent (type 1) diabetes mellitus. Implications for diagnosis and therapy.Clinical reviews in allergy & immunology · 2000Review
- Immune mechanisms that regulate susceptibility to autoimmune type I diabetes.Clinical reviews in allergy & immunology · 2000Review
- Temporal relationship between immune cell influx and the expression of inducible nitric oxide synthase, interleukin-4 and interferon-gamma in pancreatic islets of NOD mice following adoptive transfer of diabetic spleen cells.The Histochemical journal · 2000Article
- The role of environmental factors in insulin-dependent diabetes mellitus: an unresolved issue.Environmental health perspectives · 1999Review
- Prevention of autoimmune diabetes by intramuscular gene therapy with a nonviral vector encoding an interferon-gamma receptor/IgG1 fusion protein.Gene therapy · 1999Article
- An immunohistochemical study of macrophage influx and the co-localization of inducible nitric oxide synthase in the pancreas of non-obese diabetic (NOD) mice during disease acceleration with cyclophosphamide.The Histochemical journal · 1999Article
- Regulation of inducible nitric oxide synthase expression in beta cells by environmental factors: heavy metals.The Biochemical journal · 1999Article
- Inducible nitric oxide synthase in human diseases.Clinical and experimental immunology · 1998Review
- 1,25-Dihydroxyvitamin D3 restores sensitivity to cyclophosphamide-induced apoptosis in non-obese diabetic (NOD) mice and protects against diabetes.Clinical and experimental immunology · 1998Article
- Active stage of autoimmune diabetes is associated with the expression of a novel cytokine, IGIF, which is located near Idd2.The Journal of clinical investigation · 1997Article
- Inducible nitric oxide synthase in pancreatic islets of the non-obese diabetic mouse: a light and confocal microscopical study of its ontogeny, co-localization and up-regulation following cytokine administration.The Histochemical journal · 1997Article
- The role of interleukin-1 in the pathogenesis of IDDM.Diabetologia · 1996Review
- Interleukin-12 gene expression is associated with rapid development of diabetes mellitus in non-obese diabetic mice.Diabetologia · 1996Article
- Insulitis and islet-cell antibody formation in rats with experimentally reduced beta-cell mass.Diabetologia · 1995Article
- Alternative Medicine in Diabetes - Role of Angiogenesis, Oxidative Stress, and Chronic Inflammation.The review of diabetic studies : RDSReview
- Ribavirin in cancer immunotherapies: controlling nitric oxide augments cytotoxic lymphocyte function.Neoplasia (New York, N.Y.)Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In pancreatic lesions of non-obese diabetic (NOD) mice the expression of inducible nitric oxide synthase (iNOS) and of the cytokines interferon-gamma and interleukin-4 were studied. Strong iNOS expression as determined at the level of transcription, translation and of enzyme activity was associated with destructive insulitis as seen 8-10 days after cyclophosphamide treatment of 70- to 80-day-old female NOD mice. Immunohistochemistry showed iNOS associated with infiltrating macrophages but not in endocrine cells. The enhancement of iNOS after cyclophosphamide correlated with an increase of T-helper type 1 (Th1) associated interferon-gamma expression while T-helper type 2 (Th2) associated interleukin-4 was the dominant cytokine prior to cyclophosphamide and after diabetes onset. We conclude that insulitis in young NOD mice is carried by Th2 cells while cyclophosphamide enhanced insulitis is determined by Th1 cells. Macrophages show two different functional states in insulitis; strong iNOS expression in macrophages is associated with destructive insulitis.
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