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Absence of IL-1 signaling and reduced inflammatory response in IL-1 type I receptor-deficient mice

Academic Article
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Overview

authors

  • Labow, M.
  • Shuster, D.
  • Zetterstrom, M.
  • Nunes, P.
  • Terry, R.
  • Cullinan, E. B.
  • Bartfai, Tamas
  • Solorzano, C.
  • Moldawer, L. L.
  • Chizzonite, R.
  • McIntyre, K. W.

publication date

  • September 1997

journal

  • Journal of Immunology  Journal

abstract

  • IL-1alpha and IL-1beta are potent inflammatory cytokines that contribute to a number of normal physiologic processes and to the development of a number of inflammatory diseases. Two IL-1R, the type I and type II receptors, have been identified. This work describes the derivation and characterization of mice deficient in expression of the type I IL-1R (IL-1RI). IL-1RI-deficient mice were viable and fertile, but failed to respond to IL-1 in a variety of assays, including IL-1-induced IL-6 and E-selectin expression and IL-1-induced fever. Similar to IL-1beta-deficient mice, IL-1RI-deficient mice had a reduced acute phase response to turpentine. In contrast, IL-1RI-deficient mice had a reduced delayed-type hypersensitivity response and were highly susceptible to infection by Listeria monocytogenes. These data demonstrate that the IL-1RI is essential for all IL-1-mediated signaling events examined, and that both IL-1alpha and IL-1beta are critical to the animals' response to injury and infection. These data also demonstrate that IL-1 function is not required for normal development or homeostasis.

subject areas

  • Acute-Phase Reaction
  • Animals
  • Cells, Cultured
  • Disease Susceptibility
  • E-Selectin
  • Female
  • Fever
  • Fibroblasts
  • Gene Targeting
  • Hypersensitivity, Delayed
  • Inflammation
  • Interleukin-1
  • Interleukin-6
  • Listeriosis
  • Male
  • Mice
  • Mice, Knockout
  • Receptors, Interleukin-1
  • Receptors, Interleukin-1 Type I
  • Signal Transduction
  • Turpentine
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 9278338
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Additional Document Info

start page

  • 2452

end page

  • 2461

volume

  • 159

issue

  • 5

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