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Cells in Accelerated, But Not Spontaneous, Diabetes in Nonobese Diabetic Mice1
* St. Vincent’s Institute of Medical Research, Fitzroy, Australia,
Walter and Eliza Hall Institute of Medical Research, Parkville, Australia; and
Department of Microbiology and Infectious Diseases and Julia McFarlane Diabetes Research Center, Faculty of Medicine, University of Calgary, Alberta, Canada
Fas (CD95) is a potential mechanism of pancreatic 
cell death in type 1 diabetes. cells do not constitutively express Fas but it is induced by cytokines. The hypothesis of this study is that Fas expression should be measurable on cells for them to be killed by this mechanism. We have previously reported that up to 5% of cells isolated from nonobese diabetic (NOD) mice are positive for Fas expression by flow cytometry using autofluorescence to identify cells. We have now found that these are not cells but contaminating dendritic cells, macrophages, and B lymphocytes. In contrast cells isolated from NODscid mice that are recipients of T lymphocytes from diabetic NOD mice express Fas 18–25 days after adoptive transfer but before development of diabetes. Fas expression on cells was also observed in BDC2.5, 8.3, and 4.1 TCR-transgenic models of diabetes in which diabetes occurs more rapidly than in unmodified NOD mice. In conclusion, Fas is observed on cells in models of diabetes in which rapid cell destruction occurs. Its expression is likely to reflect differences in the intraislet cytokine environment compared with the spontaneous model and may indicate a role for this pathway in cell destruction in rapidly progressive models.
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