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Published online before print May 3, 2004

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0503247

Received for publication May 28, 2003.
Revised March 23, 2004.
Accepted for publication March 26, 2004.

Article

IFN- inhibits the proliferation of allergen-activated T lymphocytes from atopic, asthmatic patients by inducing Fas/FasL-mediated apoptosis

Virginia De Rose ^*@, Paola Cappello , Valentina Sorbello ^*, Barbara Ceccarini ^*, Federica Gani ^*, Marita Bosticardo , Stefania Fassio ^*, and Francesco Novelli

*Respiratory Disease Division, Department of Clinical and Biological Sciences, and Department of Medicine and Experimetal Oncology, University of Turin, Italy; and Center for Experimental Research and Medical Studies (CeRMS), S. Giovanni Battista Hospital, Turin, Italy

^@ To whom correspondence should be addressed. E-mail: virginia.derose{at}unito.it.

	Abstract

The defect in interferon- (IFN-) production that results in a T helper cell type 2-dominated response may be responsible for a decrease in the apoptosis of allergen-activated T cells in asthma. We investigated the effect of recombinant IFN- on proliferation, Fas/Fas ligand (FasL) expression, and apoptosis in allergen-stimulated peripheral blood mononuclear cells obtained from atopic, asthmatic patients and nonatopic, control subjects. The addition of IFN- at the start of cultures markedly inhibited the proliferative response to a specific allergen in cells from all asthmatic patients, whereas no change was observed in cells from nonatopic, control subjects. IFN- induced an increase in the expression of Fas and FasL by allergen-stimulated CD4+ T cells from asthmatic patients and caused the apoptosis of these cells. A Fas-blocking monoclonal antibody prevented the inhibitory effect of IFN- on allergen-induced proliferation. These results suggest that IFN- inhibits the proliferation of allergen-stimulated CD4+ T cells from atopic, asthmatic patients by inducing the surface expression of Fas and FasL, which in turn triggers their apoptotic program. The defect in IFN- production involved in the allergic, immune response may therefore be responsible for a decrease in apoptosis of allergen-activated T lymphocytes in the airways of atopic, asthmatic patients.

Key Words: asthma • allergy • inflammation • cytokines

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