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International Journal of Experimental Pathology logoLink to International Journal of Experimental Pathology
. 1998 Oct;79(5):313–320. doi: 10.1046/j.1365-2613.1998.670398.x

Interferon-γ plays a role in pancreatic islet-cell destruction of reovirus type 2 -induced diabetes–like syndrome in DBA/1 suckling mice

T HAYASHI 1, M MORIMOTO 1, H IWATA 2, T ONODERA 3
PMCID: PMC3220239  PMID: 10193314

Abstract

Reovirus type 2 (Reo-2) infection in DBA/1 suckling mice causes insulitis, which leads to pancreatic islet-cell destruction,resulting in a diabetes–like syndrome. T-helper (Th)1 cytokines are thought to play a key role in islet inflammation in insulin-dependent diabetes mellitus. We examined this hypothesis in the Reo-2-induced diabetes–like syndrome. We used reverse transcriptase polymerase chain reaction (PCR) and quantitative PCR techniques to examine mRNA expression of interferon (IFN)-γ (Th1 type cytokine), and interleukin (IL)-4 (Th2 type cytokine) in splenic cells. We observed that in Reo-2 infected mice the level of IFN-γ expression increases with the development of insulitis, whereas expression of message for IL-4 is minimal to detectable with the immuno-inflammatory process 10 days after infection. The treatment of monoclonal antibody (mAb) against mouse IFN-γ during the expansion phase of insulitis (5–9 days after infection) inhibited the development of insulitis and the elevation of blood glucose concentrations in a dose dependent manner. Furthermore altered CD4+/CD8+ cell ratio compared with uninfected mice in the splenic cells by the infection was recovered to the ratio of uninfected mice by the treatment of mAb against mouse IFN-γ, suggesting normalization of T cell balance in immune system. These results suggest that Reo-2-triggered autoimmune insulitis may be mediated by Th1 lymphocytes and IFN-γ may play a role in islet inflammation leading to islet cell destruction.

Keywords: IDDM, IFN-γ, mouse, reovirus, Th1 cell


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