Nature Communications (Jul 2016)

Deletion of Wiskott–Aldrich syndrome protein triggers Rac2 activity and increased cross-presentation by dendritic cells

  • Marisa A. P. Baptista,
  • Marton Keszei,
  • Mariana Oliveira,
  • Karen K. S. Sunahara,
  • John Andersson,
  • Carin I. M. Dahlberg,
  • Austen J. Worth,
  • Agne Liedén,
  • I-Chun Kuo,
  • Robert P. A. Wallin,
  • Scott B. Snapper,
  • Liv Eidsmo,
  • Annika Scheynius,
  • Mikael C. I. Karlsson,
  • Gerben Bouma,
  • Siobhan O. Burns,
  • Mattias N. E. Forsell,
  • Adrian J. Thrasher,
  • Susanne Nylén,
  • Lisa S. Westerberg

DOI
https://doi.org/10.1038/ncomms12175
Journal volume & issue
Vol. 7, no. 1
pp. 1 – 15

Abstract

Read online

Wiskott–Aldrich syndrome (WAS) is a severe X-linked primary immunodeficiency syndrome. Here, the authors show that loss of WAS gene in dendritic cells results in increased activity of Rac2, increase of phagosomal pH, and more efficient cross-presentation.