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

R. Trueb, G. Brown, C. Van Huffel, A. Poltorak, M. Valdez-Silva, B. Beutler

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

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

Original languageEnglish (US)
Pages (from-to)239-247
Number of pages9
JournalJournal of Inflammation
Volume45
Issue number4
StatePublished - 1995

Keywords

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

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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