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Blood, 15 December 2000, Vol. 96, No. 13, pp. 4285-4292
IMMUNOBIOLOGY
Interferon  prevents spontaneous apoptosis of clonal Th2
cells associated with chronic hypereosinophilia
Liliane Schandené,
Florence Roufosse,
Aurore de Lavareille,
Patrick Stordeur,
André Efira,
Bernard Kennès,
Elie Cogan, and
Michel Goldman
From the Department of Immunology, Hôpital
Erasme; Department of Internal Medicine, Hôpital Erasme; and
Department of Medicine, CHU Saint-Pierre, Université Libre de
Bruxelles, Brussels, Belgium; and CHU Vésale,
Montigny-le-Tilleul, Belgium.
A recent study identified a clonal expansion of
CD3 CD4+cells secreting Th2-type cytokines in
4 patients with chronic hypereosinophilia. Because interferon  (IFN-) is used in the therapy of the idiopathic hypereosinophilic
syndrome, the effects of this cytokine on the survival of clonal Th2
cells isolated from the blood of 2 patients were determined. First,
these cells displayed a high rate of spontaneous apoptosis on culture
in cytokine-free medium and were also sensitive to Fas-mediated
apoptosis induced by soluble Fas ligand. Addition of IFN- or
interleukin-2 (IL-2) to culture medium resulted in significant
protection against spontaneous but not Fas-induced apoptosis. Although
spontaneous apoptosis of the clonal Th2 cells was clearly associated
with down-regulation of both bcl-2 and bcl-xL levels,
IFN- had no significant effect on the expression of these
antiapoptotic proteins, whereas addition of IL-2 resulted in higher
levels of bcl-2. On the other hand, IFN- decreased the numbers of
cells with disrupted mitochondrial transmembrane potential both during
spontaneous apoptosis and after exposure to protoporphyrin IX. Thus,
IFN- might promote the survival of clonal Th2 cells, an effect that
could be relevant to the therapeutic approach for patients with chronic
hypereosinophilia caused by clonal expansion of Th2-type cells.
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