The Wiskott-Aldrich syndrome protein regulates nuclear translocation of NFAT2 and NF-kappa B (RelA) independently of its role in filamentous actin polymerization and actin cytoskeletal rearrangement

J Immunol. 2005 Mar 1;174(5):2602-11. doi: 10.4049/jimmunol.174.5.2602.

Abstract

Effector functions mediated by NK cells involve cytotoxicity and transcription-dependent production and release of cytokines and chemokines. Although the JAK/STAT pathway mediates lymphokine-induced transcriptional regulation in NK cells, very little is known about transcriptional regulation induced during cell-cell contact. We demonstrate that the Wiskott-Aldrich syndrome protein (WASp) is an important component for integration of signals leading to nuclear translocation of NFAT2 and NF-kappaB (RelA) during cell-cell contact and NKp46-dependent signaling. This WASp function is independent of its known role in F-actin polymerization and cytoskeletal rearrangement. Absence of WASp results in decreased accumulation of calcineurin, WASp-interacting protein, and molecules upstream of calcium mobilization, i.e., activated ZAP70 and phospholipase C-gamma1, in the disorganized NK cell immune synapse. Production of GM-CSF, but not IFN-gamma, is decreased, while natural cytotoxicity of Wiskott-Aldrich syndrome-NK cells is maintained. Our results indicate that WASp independently regulates its dual functions, i.e., actin cytoskeletal remodeling and transcription in NK cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Actins / metabolism*
  • Active Transport, Cell Nucleus / genetics
  • Cell Communication / genetics
  • Cell Communication / immunology
  • Cell Line, Transformed
  • Cell Nucleus / metabolism*
  • Clone Cells
  • Cytoskeleton / metabolism*
  • Cytotoxicity, Immunologic / genetics
  • DNA-Binding Proteins / metabolism*
  • Granulocyte-Macrophage Colony-Stimulating Factor / antagonists & inhibitors
  • Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis
  • Humans
  • Interferon-gamma / biosynthesis
  • Killer Cells, Natural / enzymology
  • Killer Cells, Natural / immunology
  • Killer Cells, Natural / metabolism
  • Lymphocyte Activation / genetics
  • Membrane Glycoproteins / physiology
  • Membrane Microdomains / enzymology
  • Membrane Microdomains / immunology
  • Membrane Microdomains / metabolism
  • NF-kappa B / metabolism*
  • NFATC Transcription Factors
  • Natural Cytotoxicity Triggering Receptor 1
  • Nuclear Proteins / metabolism*
  • Phospholipase C gamma
  • Proteins / genetics
  • Proteins / physiology*
  • Receptors, Immunologic / physiology
  • Signal Transduction / genetics
  • Signal Transduction / immunology
  • Transcription Factor RelA
  • Transcription Factors / metabolism*
  • Type C Phospholipases / antagonists & inhibitors
  • Type C Phospholipases / metabolism
  • Wiskott-Aldrich Syndrome / genetics
  • Wiskott-Aldrich Syndrome / immunology*
  • Wiskott-Aldrich Syndrome / metabolism*
  • Wiskott-Aldrich Syndrome Protein

Substances

  • Actins
  • DNA-Binding Proteins
  • Membrane Glycoproteins
  • NCR1 protein, human
  • NF-kappa B
  • NFATC Transcription Factors
  • Natural Cytotoxicity Triggering Receptor 1
  • Nuclear Proteins
  • Proteins
  • Receptors, Immunologic
  • Transcription Factor RelA
  • Transcription Factors
  • WAS protein, human
  • Wiskott-Aldrich Syndrome Protein
  • Interferon-gamma
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Type C Phospholipases
  • Phospholipase C gamma