GSK-3 mediates differentiation and activation of proinflammatory dendritic cells

Blood. 2007 Feb 15;109(4):1584-92. doi: 10.1182/blood-2006-06-028951. Epub 2006 Oct 10.

Abstract

The key components of the intracellular molecular network required for the expression of a specific function of dendritic cells (DCs) are as yet undefined. Using an in vitro model of human monocyte-derived DC differentiation, this study investigates the role of glycogen synthase kinase 3 (GSK-3), a multifunctional enzyme critical for cellular differentiation, apoptosis, self-renewal, and motility, in this context. We demonstrate that GSK-3 (1) inhibits macrophage development during differentiation of DCs, (2) is constitutively active in immature DCs and suppresses spontaneous maturation, and (3) acquires a proinflammatory functional status mediating high levels of IL-12, IL-6, and TNF-alpha secretion, and partially inhibits IL-10 in the context of DC activation. In particular, GSK-3 enhances IL-12p35 mRNA expression and thus the production of the proinflammatory cytokine IL-12p70 by integrating the activities of other kinases priming GSK-3 targets and the inhibitory effects of Akt-1. GSK-3 may therefore act as a key integrator of activating and inhibitory pathways involved in proinflammatory DC differentiation and activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Differentiation / immunology*
  • Cells, Cultured
  • Dendritic Cells / immunology*
  • Glycogen Synthase Kinase 3 / physiology*
  • Humans
  • Inflammation / immunology*
  • Interleukin-12 / genetics
  • Interleukins / genetics
  • Macrophages / cytology
  • Proto-Oncogene Proteins c-akt / physiology
  • Transcription, Genetic
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Interleukins
  • Tumor Necrosis Factor-alpha
  • Interleukin-12
  • Proto-Oncogene Proteins c-akt
  • Glycogen Synthase Kinase 3