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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Reduced incidence and delayed onset of diabetes in perforin-deficient nonobese diabetic mice.

To investigate the role of T cell-mediated, perforin-dependent cytotoxicity in autoimmune diabetes, perforin-deficient mice were backcrossed with the nonobese diabetes mouse strain. It was found that the incidence of spontaneous diabetes over a 1 yr period was reduced from 77% in perforin +/+ control to 16% in perforin-deficient mice. Also, the disease onset was markedly delayed (median onset of 39.5 versus 19 wk) in the latter. Insulitis with infiltration of CD4(+) and CD8(+) T cells occurred similarly in both groups of animals. Lower incidence and delayed disease onset were also evident in perforin-deficient mice when diabetes was induced by cyclophosphamide injection. Thus, perforin-dependent cytotoxicity is a crucial effector mechanism for beta cell elimination by cytotoxic T cells in autoimmune diabetes. However, in the absence of perforin chronic inflammation of the islets can lead to diabetogenic beta cell loss by less efficient secondary effector mechanisms.[1]

References

  1. Reduced incidence and delayed onset of diabetes in perforin-deficient nonobese diabetic mice. Kägi, D., Odermatt, B., Seiler, P., Zinkernagel, R.M., Mak, T.W., Hengartner, H. J. Exp. Med. (1997) [Pubmed]
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