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Titolo:
Disease resistant, NOD-related strains reveal checkpoints of immunoregulation in the pancreas
Autore:
Rothe, H; Ito, Y; Kolb, H;
Indirizzi:
Diabet Res Inst, D-80804 Munich, Germany Diabet Res Inst Munich Germany D-80804 Res Inst, D-80804 Munich, Germany Univ Dusseldorf, German Diabet Res Inst, D-4000 Dusseldorf, Germany Univ Dusseldorf Dusseldorf Germany D-4000 st, D-4000 Dusseldorf, Germany
Titolo Testata:
JOURNAL OF MOLECULAR MEDICINE-JMM
fascicolo: 4, volume: 79, anno: 2001,
pagine: 190 - 197
SICI:
0946-2716(200105)79:4<190:DRNSRC>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
NONOBESE DIABETIC MICE; NITRIC-OXIDE SYNTHASE; T-CELL CLONE; BB RATS; SELECTIVE EXPRESSION; IL-4 EXPRESSION; DENDRITIC CELLS; TH2 CELLS; INSULITIS; CYTOKINE;
Keywords:
NOD mice; NOR mice; NON mice; insulitis; interleukin-12;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Rothe, H Diabet Res Inst, Koelner Pl 1, D-80804 Munich, Germany Diabet ResInst Koelner Pl 1 Munich Germany D-80804 ich, Germany
Citazione:
H. Rothe et al., "Disease resistant, NOD-related strains reveal checkpoints of immunoregulation in the pancreas", J MOL MED-J, 79(4), 2001, pp. 190-197

Abstract

The autoimmune diabetic NOD mouse serves as a model for human type 1 diabetes. Disease development is due to islet beta cell destruction in the context of immune cell infiltration of islets and inflammatory changes throughout the pancreas. In the present study we tried to identify immune reactivitypatterns in the pancreas associated with diabetes resistance in NOD-related mouse strains. The pancreata of diabetes-prone female NOD/LtJ, NOD/Bom and of genetically related but diabetes-resistant strains; NOR, NON, NON.NOD-H2(g7), NOD.NON-H-2(nbl) were obtained at the age of 70 days for semiquantitative analysis of insulitis and of mRNA expression by reverse transcriptase PCR, In addition, the response to a single dose of cyclophosphamide for synchronizing and accelerating the progression of insulitis was determined. The progression of insulitis and immune gene expression in response to cyclophosphamide revealed characteristic differences between the six strains. NOD/LtJ and NOD/Bom mice were found significantly to upregulate pancreatic IL-12p40 and IL-18 expression after cyclophosphamide treatment, followed by an increase in IFN-gamma mRNA levels. In contrast, the two MHC-haplotype H-2(nbl) expressing strains either upregulated neither IL-12/IL-18 nor IFN-gamma gene expression. The two strains sharing MHC haplotype H-2(g7) expression with NOD did respond to cyclophosphamide with IL-12p40/IL-18 gene expression. However, NON,NOD H-2(g7) mice failed to progress to IFN-gamma gene expression. NOR mice progressed to IFN-gamma expression but exhibited sustained IL-4 gene expression. Only severe intra-insulitis was associated with the expression of inducible NO synthase, The comparison of diabetes-prone anddiabetes-resistant strains revealed three checkpoints of;immune regulationin the pancreas. The earliest checkpoint is the induction of an IL-12p40/IL-18 response in innate immune or antigen-presenting;no cells. The next level of control is at the induction of IFN-gamma gene expression, and a thirdcheckpoint is the maintenance or loss of antagonistic Th2 type reactions.

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Documento generato il 01/04/20 alle ore 20:31:38