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

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

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.

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Bibliographic Details
Main Authors: 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
Format: article
Language:EN
Published: Nature Portfolio 2016
Subjects:
Science
Q
Online Access:https://doaj.org/article/b30cb5531b534a4c9f3e0c5bebf69da8
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Summary: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.

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