Disturbances in apoptosis or in the clearance of apoptotic material might r
esult in increased presentation of autoantigens which could be relevant to
the pathogenesis of SLE. Data concerning defects in apoptosis in SLE are co
nflicting. To determine whether intrinsic defects in apoptosis induction oc
cur in SLE irrespective of disease activity, we examined anti-CD3 and anti-
Fas-induced apoptosis in vitro in SLE patients with inactive disease. Isola
ted peripheral blood lymphocytes (PBL) from 13 SLE patients and 14 healthy
controls were incubated with anti-CD3, and, subsequently, after up-regulati
on of membrane Fas following anti-CD3 incubation, with anti-Fas. Expression
of Fas and levels of apoptosis as detected by annexin V and propidium iodi
de staining were assessed by flow cytometry before and after the respective
incubations. Fas expression on freshly isolated lymphocytes of SLE patient
s was increased whereas levels of circulating apoptotic cells were comparab
le between patients and controls. Stimulation with anti-CD3 resulted in up-
regulation of membrane Fas in patients and in controls. In vitro induction
of apoptosis by anti-CD3 as well as by anti-Fas occurred both in SLE patien
ts and controls, and was higher in SLE patients after incubation with anti-
CD3 as well as with anti-Fas. We conclude that Fas expression and in vitro
induction of apoptosis are increased in SLE even in the absence of disease
activity.