Type I Interferon Sensitizes Lymphocytes to Apoptosis and Reduces Resistance to Listeria Infection

doi:10.1084/jem.20040769

Published online 9 August 2004 doi:10.1084/jem.20040769
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 4, 535-540

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Type I Interferon Sensitizes Lymphocytes to Apoptosis and Reduces Resistance to Listeria Infection

Javier A. Carrero, Boris Calderon, and Emil R. Unanue

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110

Address correspondence to Emil R. Unanue, Dept. of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Ave., St. Louis, MO 63110. Phone: (314) 362-7442; Fax: (314) 362-4096; email: unanue{at}pathology.wustl.edu

Infection with Listeria monocytogenes causes lymphocyte apoptosisthat is mediated by the actions of the pore-forming virulencefactor listeriolysin O (LLO). Previous work showed that activatedlymphocytes were highly sensitive to LLO-induced apoptosis,whereas resting lymphocytes were less susceptible. We now showthat mice deficient in the type I interferon (IFN) receptorwere more resistant to Listeria infection and had less apoptoticlesions than wild-type counterparts. Furthermore, treatmentof resting splenic lymphocytes with recombinant IFN- ${alpha}$ A enhancedtheir susceptibility to LLO-induced apoptosis. Together, thesedata suggest that type I IFN signaling is detrimental to handlingof a bacterial pathogen and may enhance the susceptibility oflymphocytes undergoing apoptosis in response to bacterial pore-formingtoxins.

Key Words: apoptosis • cytokines • Listeria • inflammation • T lymphocytes

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