Activation of Interferon-γ Inducing Factor Mediated by Interleukin-1β Converting Enzyme

Yong Gu(Vertex Pharmaceuticals (United States)), Keisuke Kuida(Tokyo Metropolitan Institute of Medical Science), Hiroko Tsutsui(Hyogo Medical University), George Ku(Vertex Pharmaceuticals (United States)), Kathy Hsiao(Vertex Pharmaceuticals (United States)), Mark Fleming(Vertex Pharmaceuticals (United States)), Nobuki Hayashi(Hyogo Medical University), Kazuya Higashino(Hyogo Medical University), Haruki Okamura(Hyogo Medical University), Kenji Nakanishi(Hyogo Medical University), Masashi Kurimoto(Hayashibara (Japan)), Tadao Tanimoto(Hayashibara (Japan)), Richard A. Flavell(Howard Hughes Medical Institute), Vicki L. Sato(Vertex Pharmaceuticals (United States)), Matthew W. Harding(Vertex Pharmaceuticals (United States)), David J. Livingston(Vertex Pharmaceuticals (United States)), Michael Su(Vertex Pharmaceuticals (United States))
Science
January 10, 1997
10.1126/science.275.5297.206
Cited by 1,156

Abstract

The interleukin-1beta (IL-1beta) converting enzyme (ICE) processes the inactive IL-1beta precursor to the proinflammatory cytokine. ICE was also shown to cleave the precursor of interferon-gamma inducing factor (IGIF) at the authentic processing site with high efficiency, thereby activating IGIF and facilitating its export. Lipopolysaccharide-activated ICE-deficient (ICE-/-) Kupffer cells synthesized the IGIF precursor but failed to process it into the active form. Interferon-gamma and IGIF were diminished in the sera of ICE-/- mice exposed to Propionibacterium acnes and lipopolysaccharide. The lack of multiple proinflammatory cytokines in ICE-/- mice may account for their protection from septic shock.

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