Vav Proteins Are Key Regulators of Card9 Signaling for Innate Antifungal Immunity
Susanne Roth(Heidelberg University), Hanna Bergmann(TUM Klinikum), Martin Jaeger(Radboud University Nijmegen), Assa Yeroslaviz(Max Planck Institute of Biochemistry), Konstantin Neumann(TUM Klinikum), Paul-Albert Koenig(TUM Klinikum), Clarissa Prazeres da Costa(TUM Klinikum), Lesley Vanes(The Francis Crick Institute), Vinod Kumar(University Medical Center Groningen), Melissa D. Johnson(Duke Medical Center), Mauricio Menacho-Márquez(Universidad de Salamanca), Bianca Habermann(Max Planck Institute of Biochemistry), Victor L. J. Tybulewicz(The Francis Crick Institute), Mihai G. Netea(Radboud University Nijmegen), Xosé R. Bustelo(Universidad de Salamanca), Jürgen Ruland(German Cancer Research Center)
Cited by 75Open Access
Abstract
animals with extreme susceptibility to fungi. In this context, Vav3 is the single most important Vav in mice, and a polymorphism in human VAV3 is associated with susceptibility to candidemia in patients. Our results reveal a molecular mechanism for CLR-mediated Card9 regulation that controls innate immunity to fungal infections.