Caspase-8 prevents sustained activation of NF-kappaB in monocytes undergoing macrophagic differentiation

Blood. 2007 Feb 15;109(4):1442-50. doi: 10.1182/blood-2006-03-011585. Epub 2006 Oct 17.

Abstract

Caspases have demonstrated several nonapoptotic functions including a role in the differentiation of specific cell types. Here, we show that caspase-8 is the upstream enzyme in the proteolytic caspase cascade whose activation is required for the differentiation of peripheral-blood monocytes into macrophages. On macrophage colony-stimulating factor (M-CSF) exposure, caspase-8 associates with the adaptor protein Fas-associated death domain (FADD), the serine/threonine kinase receptor-interacting protein 1 (RIP1) and the long isoform of FLICE-inhibitory protein FLIP. Overexpression of FADD accelerates the differentiation process that does not involve any death receptor. Active caspase-8 cleaves RIP1, which prevents sustained NF-kappaB activation, and activates downstream caspases. Together these data identify a role for caspase-8 in monocytes undergoing macrophagic differentiation, that is, the enzyme activated in an atypical complex down-regulates NF-kappaB activity through RIP1 cleavage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Caspase 8 / metabolism
  • Caspase 8 / physiology*
  • Cell Differentiation*
  • Cell Line, Tumor
  • Fas-Associated Death Domain Protein / metabolism
  • Humans
  • Macrophage Colony-Stimulating Factor / pharmacology
  • Macrophages / cytology*
  • Monocytes / cytology*
  • NF-kappa B / metabolism*
  • Nuclear Pore Complex Proteins / metabolism*
  • RNA-Binding Proteins / metabolism*

Substances

  • AGFG1 protein, human
  • FADD protein, human
  • Fas-Associated Death Domain Protein
  • NF-kappa B
  • Nuclear Pore Complex Proteins
  • RNA-Binding Proteins
  • Macrophage Colony-Stimulating Factor
  • Caspase 8