There is increasing evidence that inappropriate induction of apoptosis in p
ancreatic beta-cells may precede the development of type 1 diabetes in anim
al models and in man. One mechanism by which this has been proposed to occu
r involves up-regulation of the death receptor Fas on beta-cells, resulting
in apoptosis of the Fas-bearing beta-cells upon ligation of the receptor.
We have examined this hypothesis in isolated human islets of Langerhans and
show that--in contrast to data obtained with rodent beta-cells-expression
of Fas per se is not sufficient to allow induction of apoptosis upon additi
on of agonistic anti-Fas serum.