Abstract | BACKGROUND: RESULTS:
Inflammation and periacinar oedema peaked on day 3 and were replaced by a focal inflammation, but infected cells were rare. The islets were spared in C57BL mice. Insulitis normally seen in non-obese diabetic (NOD) mice was accelerated, but infected NOD mice did not become glycosuric. Isotypes of total and autoreactive antibodies suggested a shift to a Th 1 response ( IgG2a) in all MCMV-infected mice. MCMV-induced pancreatitis was not affected by MHC genes but was similar or less severe in BALB/c mice. As these lack the Cmv1 gene, which provides a protective natural killer (NK) cell response in C57BL congenic mice, the C57BL background may carry a pancreatitis susceptibility gene able to counter NK-mediated restriction of viral replication. Consistently, congenic mice expressing Cmvl on a BALB/c background did not display pancreatitis, unless depleted of NK cells. In vivo treatment with soluble cytokine receptors suggested that interleukin 1 (IL-1) and/or tumour necrosis factor alpha contribute to acinar necrosis in C57BL mice.
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Authors | P Price, A G Baxter, R N Allcock, J M Papadimitriou |
Journal | European journal of clinical investigation
(Eur J Clin Invest)
Vol. 28
Issue 7
Pg. 546-53
(Jul 1998)
ISSN: 0014-2972 [Print] England |
PMID | 9726035
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Autoantibodies
- Interleukin-1
- Receptors, Interleukin-1
- Receptors, Tumor Necrosis Factor
- Tumor Necrosis Factor-alpha
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Topics |
- Animals
- Autoantibodies
(blood)
- Cytomegalovirus
(pathogenicity, physiology)
- Cytomegalovirus Infections
(pathology)
- Diabetes Mellitus, Type 1
(virology)
- Female
- Humans
- Hypergammaglobulinemia
(pathology, virology)
- Interleukin-1
(physiology)
- Islets of Langerhans
(pathology, virology)
- Killer Cells, Natural
(immunology)
- Liver
(pathology, virology)
- Lymphocyte Depletion
- Mice
- Mice, Inbred BALB C
- Mice, Inbred C57BL
- Mice, Inbred NOD
- Necrosis
- Pancreas
(pathology, virology)
- Pancreatitis
(pathology, virology)
- Receptors, Interleukin-1
(administration & dosage, physiology)
- Receptors, Tumor Necrosis Factor
(administration & dosage, physiology)
- Tumor Necrosis Factor-alpha
(physiology)
- Virus Replication
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