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

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.

Pubmed ID: 9278338 RIS Download

Mesh terms: 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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Associated grants

  • Agency: NICHD NIH HHS, Id: HD07855
  • Agency: NIGMS NIH HHS, Id: R01-GM-40586

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