Tumor necrosis factor-α- and interleukin-1-induced cellular responses: Coupling proteomic and genomic information

Academic Article


  • The pro-inflammatory cytokines, Tumor Necrosis Factor-alpha (TNFα) and Interleukin-1 (IL-1) mediate the innate immune response. Dysregulation of the innate immune response contributes to the pathogenesis of cancer, arthritis, and congestive heart failure. TNFα- and IL-1-induced changes in gene expression are mediated by similar transcription factors; however, TNFα and IL-1 receptor knock-out mice differ in their sensitivities to a known initiator (lipopolysaccharide, LPS) of the innate immune response. The contrasting responses to LPS indicate that TNFα and IL-1 regulate different processes. A large-scale proteomic analysis of TNFα- and IL-1-induced responses was undertaken to identify processes uniquely regulated by TNFα and IL-1. When combined with genomic studies, our results indicate that TNFα, but not IL-1, mediates cell cycle arrest. © 2007 American Chemical Society.
  • Authors

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    Digital Object Identifier (doi)

    Author List

  • Ott LW; Resing KA; Sizemore AW; Heyen JW; Cocklin RR; Pedrick NM; Woods HC; Chen JY; Goebl MG; Witzmann FA
  • Start Page

  • 2176
  • End Page

  • 2185
  • Volume

  • 6
  • Issue

  • 6