Toll IL-1 receptors differ in their ability to promote the stabilization of adenosine and uridine-rich elements containing mRNA

J Immunol. 2004 Aug 15;173(4):2755-61. doi: 10.4049/jimmunol.173.4.2755.

Abstract

Several ligands for Toll IL-1R (TIR) family are known to promote stabilization of a subset of short-lived mRNAs containing AU-rich elements (AREs) in their 3' untranslated regions. It is now evident however, that members of the TIR family may use distinct intracellular signaling pathways to achieve a spectrum of biological end points. Using human embryonic kidney 293 cells transfected to express different TIRs we now report that signals initiated through IL-1R1 or TLR4 but not TLR3 can promote the stabilization of unstable chemokine mRNAs. Similar results were obtained when signaling from endogenous receptors was examined using a mouse endothelial cell line (H5V). The ability of TIR family members to stabilize ARE-containing mRNAs results from their differential use of signaling adaptors MyD88, MyD88 adaptor-like protein, Toll receptor IFN-inducing factor (Trif), and Trif-related adaptor molecule. Overexpression of MyD88 or MyD88 adaptor-like protein was able to promote enhanced stability of ARE-containing mRNA, whereas Trif and Trif-related adaptor molecule exhibited markedly reduced capacity. Hence the ability of TIRs to signal stabilization of mRNA appears to be linked to the MyD88-dependent signaling pathway.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3' Untranslated Regions
  • Adaptor Proteins, Signal Transducing
  • Adaptor Proteins, Vesicular Transport / immunology
  • Adaptor Proteins, Vesicular Transport / metabolism
  • Adenosine / metabolism*
  • Animals
  • Antigens, Differentiation / immunology
  • Antigens, Differentiation / metabolism
  • Blotting, Western
  • Cell Line
  • Chemokines / biosynthesis
  • Chemokines / genetics
  • Humans
  • In Situ Hybridization
  • Membrane Glycoproteins / immunology
  • Membrane Glycoproteins / metabolism*
  • Myeloid Differentiation Factor 88
  • RNA, Messenger*
  • Receptors, Cell Surface / immunology
  • Receptors, Cell Surface / metabolism*
  • Receptors, Immunologic / immunology
  • Receptors, Immunologic / metabolism
  • Receptors, Interleukin-1 / immunology
  • Receptors, Interleukin-1 / metabolism*
  • Receptors, Interleukin-1 Type I
  • Signal Transduction / physiology
  • Toll-Like Receptor 3
  • Toll-Like Receptor 4
  • Toll-Like Receptors
  • Transfection
  • Uridine / metabolism*

Substances

  • 3' Untranslated Regions
  • Adaptor Proteins, Signal Transducing
  • Adaptor Proteins, Vesicular Transport
  • Antigens, Differentiation
  • Chemokines
  • MYD88 protein, human
  • Membrane Glycoproteins
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • RNA, Messenger
  • Receptors, Cell Surface
  • Receptors, Immunologic
  • Receptors, Interleukin-1
  • Receptors, Interleukin-1 Type I
  • TIRAP protein, human
  • TLR3 protein, human
  • TLR4 protein, human
  • Toll-Like Receptor 3
  • Toll-Like Receptor 4
  • Toll-Like Receptors
  • Adenosine
  • Uridine