HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Published online before print May 3, 2004

This Article Full Text Full Text (PDF) All Versions of this Article: jlb.0503247v1 76/2/423    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by De Rose, V. Articles by Novelli, F. Search for Related Content PubMed PubMed Citation Articles by De Rose, V. Articles by Novelli, F.

(Journal of Leukocyte Biology. 2004;76:423-432.)
© 2004 by Society for Leukocyte Biology

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

Virginia De Rose^*,1, 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

¹Correspondence: Clinica di Malattie dell’Apparato Respiratorio, Dipartimento di Scienze Cliniche e Biologiche, Università di Torino, Ospedale S. Luigi Gonzaga, Regione Gonzole, 10, 10043 Orbassano (Torino), Italy. E-mail: virginia.derose{at}unito.it

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

This article has been cited by other articles:

				L. Conti, G. Regis, A. Longo, P. Bernabei, R. Chiarle, M. Giovarelli, and F. Novelli In the absence of IGF-1 signaling, IFN-{gamma} suppresses human malignant T-cell growth Blood, March 15, 2007; 109(6): 2496 - 2504. [Abstract] [Full Text] [PDF]

				J. Tong, H. S. Bandulwala, B. S. Clay, R. A. Anders, R. A. Shilling, D. D. Balachandran, B. Chen, J. V. Weinstock, J. Solway, K. J. Hamann, et al. Fas-positive T cells regulate the resolution of airway inflammation in a murine model of asthma J. Exp. Med., May 15, 2006; 203(5): 1173 - 1184. [Abstract] [Full Text] [PDF]