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From the * Ontario Cancer Institute, Toronto M5G2M9, Canada; 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
Institute of Experimental
Immunology, Department of Pathology, University of Zürich, CH-8091 Zürich, Switzerland; and
the § Department of Pathology, University of Zürich, CH-8091 Zürich, Switzerland
cell elimination by cytotoxic T cells in autoimmune diabetes. However, in
the absence of perforin chronic inflammation of the islets can lead to diabetogenic
cell loss by
less efficient secondary effector mechanisms.
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