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Expression of an adenovirally encoded lymphotoxin-beta inhibitor prevents clearance of Listeria monocytogenes in mice

Academic Article
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Overview

authors

  • Trueb, R.
  • Brown, G.
  • VanHuffel, C.
  • Poltorak, A.
  • ValdezSilva, M.
  • Beutler, Bruce

publication date

  • 1995

journal

  • Journal of Inflammation  Journal

abstract

  • The lymphotoxin (LT)-beta heterotrimer was recently identified as a molecule containing LT-alpha subunits, tethered to the cell through non-covalent association with an integral plasma membrane protein, derived from the LT-beta gene. Since knockout mutations of the LT-alpha gene yield animals that lack lymph nodes, whereas animals lacking either or both of the receptors for tumor necrosis factor (TNF) and LT-alpha homotrimers have normal lymph nodes, it has been inferred that the association between the LT-beta heterotrimer and its cognate receptor is required for lymph node ontogeny. Similarly, LT-beta and its receptor are thought to be important for development of the spleen. Since LT-alpha deficient mice lack lymph nodes, it is difficult to assess the extradevelopmental contribution of LT-beta to immune competence. To this end, we employed a strategy for the conditional blockade of LT-beta heteromer activity in normal mice. The interaction between LT-beta and its receptor is essential for the destruction of intracellular Listeria monocytogenes.

subject areas

  • Adenoviridae
  • Animals
  • Disease Susceptibility
  • Genetic Techniques
  • Genetic Vectors
  • Immune System
  • Listeria monocytogenes
  • Listeriosis
  • Lymphotoxin-alpha
  • Lymphotoxin-beta
  • Membrane Proteins
  • Mice
  • Mice, Inbred C57BL
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
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Research

keywords

  • Listeria monocytogenes
  • hepatocyte
  • immunity
  • infection
  • lymphotoxin
  • lymphotoxin-beta
  • macrophage
  • receptor
  • tumor necrosis factor
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Identity

International Standard Serial Number (ISSN)

  • 1078-7852

PubMed ID

  • 8867668
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Additional Document Info

start page

  • 239

end page

  • 247

volume

  • 45

issue

  • 4

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