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Type: Artigo de periódico
Title: Kinetics of TNF-alpha and IFN-gamma mRNA expression in islets and spleen of NOD mice
Author: Ventura-Oliveira, D.
Vilella, C.A.
Zanin, M.E.
Castro, G.M.
Moreira Filho, D.C.
Zollner, R.L.
Abstract: Insulin-dependent diabetes mellitus is caused by autoimmune destruction of pancreatic ß cells. Non-obese diabetic (NOD) mice spontaneously develop diabetes similar to the human disease. Cytokines produced by islet-infiltrating mononuclear cells may be directly cytotoxic and can be involved in islet destruction coordinated by CD4+ and CD8+ cells. We utilized a semiquantitative RT-PCR assay to analyze in vitro the mRNA expression of TNF-alpha and IFN-gamma cytokine genes in isolated islets (N = 100) and spleen cells (5 x 10(5) cells) from female NOD mice during the development of diabetes and from female CBA-j mice as a related control strain that does not develop diabetes. Cytokine mRNAs were measured at 2, 4, 8, 14 and 28 weeks of age from the onset of insulitis to the development of overt diabetes. An increase in IFN-gamma expression in islets was observed for females aged 28 weeks (149 ± 29 arbitrary units (AU), P<0.05, Student t-test) with advanced destructive insulitis when compared with CBA-j mice, while TNF-alpha was expressed in both NOD and CBA-j female islets at the same level at all ages studied. In contrast, TNF-alpha in spleen was expressed at higher levels in NOD females at 14 weeks (99 ± 8 AU, P<0.05) and 28 weeks (144 ± 17 AU, P<0.05) of age when compared to CBA-j mice. The data suggest that IFN-gamma and TNF-alpha expression in pancreatic islets of female NOD mice is associated with ß cell destruction and overt diabetes.
Subject: Diabetes
NOD mice
Pancreatic islets
Time course
Editor: Associação Brasileira de Divulgação Científica
Citation: Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 35, n. 11, p. 1347-1355, 2002.
Rights: aberto
Identifier DOI: 10.1590/S0100-879X2002001100013
Date Issue: 1-Nov-2002
Appears in Collections:Unicamp - Artigos e Outros Documentos

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