help button home button Am J Pathol Epitomics, Inc.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Torres, D.
Right arrow Articles by Erard, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Torres, D.
Right arrow Articles by Erard, F.
(American Journal of Pathology. 2005;167:1677-1687.)
© 2005 American Society for Investigative Pathology

Membrane Tumor Necrosis Factor Confers Partial Protection to Listeria Infection

David Torres*, Laure Janot*, Valerie F.J. Quesniaux*, Sergei I. Grivennikov*{dagger}, Isabelle Maillet*, Jonathon D. Sedgwick{ddagger}, Bernhard Ryffel* and Francois Erard*§

From the Transgenose Institute,* Centre National de la Recherche Scientifique, Molecular Immunology and Embryology, Orléans, France; the Laboratory of Molecular Immunology,{dagger} Engelhardt Institute of Molecular Biology, Moscow, Russia; DNAX Research Incorporated,{ddagger} Palo Alto, California; and the University of Orléans,§ Orléans, France

Tumor necrosis factor (TNF) plays a critical role in the host response to the intracellular pathogen Listeria monocytogenes (LM). TNF exists in soluble and membrane-bound forms and exhibits both unique and overlapping activities. We examined the role of membrane TNF in the absence of secreted TNF for host resistance in knockin mice in which the endogenous TNF was replaced by a regulated, noncleavable allele (mem-TNF). Macrophages expressing mem-TNF produced nitric oxide and displayed normal bactericidal activity. Although mice completely deficient in TNF (TNF–/–) succumbed to LM infection within 4 days, mem-TNF mice controlled LM infection at a low dose (104 CFU) but succumbed at a higher dose of infection (105 CFU). In contrast to complete TNF deficiency, mem-TNF mice developed confined microabscesses that expressed inducible nitric oxide synthase. The transfer of lymphocytes from immunized mem-TNF, but not TNF–/–, mice protected TNF–/– mice from fatal infection. Taken together the data suggest that in the absence of soluble TNF, the presence of membrane-expressed TNF on phagocytes and lymphocytes partially restores host defense to LM infection.




This article has been cited by other articles:


Home page
 J. Immunol.Home page
M. Forlenza, S. Magez, J. P. Scharsack, A. Westphal, H. F. J. Savelkoul, and G. F. Wiegertjes
Receptor-Mediated and Lectin-Like Activities of Carp (Cyprinus carpio) TNF-{alpha}
J. Immunol., October 15, 2009; 183(8): 5319 - 5332.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
J. Zalevsky, T. Secher, S. A. Ezhevsky, L. Janot, P. M. Steed, C. O'Brien, A. Eivazi, J. Kung, D.-H. T. Nguyen, S. K. Doberstein, et al.
Dominant-Negative Inhibitors of Soluble TNF Attenuate Experimental Arthritis without Suppressing Innate Immunity to Infection
J. Immunol., August 1, 2007; 179(3): 1872 - 1883.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
G. Spohn, R. Guler, P. Johansen, I. Keller, M. Jacobs, M. Beck, F. Rohner, M. Bauer, K. Dietmeier, T. M. Kundig, et al.
A Virus-Like Particle-Based Vaccine Selectively Targeting Soluble TNF-{alpha} Protects from Arthritis without Inducing Reactivation of Latent Tuberculosis
J. Immunol., June 1, 2007; 178(11): 7450 - 7457.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the American Society for Investigative Pathology.