Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

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

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

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
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 9278338
scroll to property group menus

Additional Document Info

start page

  • 2452

end page

  • 2461

volume

  • 159

issue

  • 5

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support