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Vav proteins are key regulators of card9 signaling for innate antifungal immunity

AutorRoth, Susanne; Bergmann, Hanna; Jaeger, Martin; Yeroslaviz, Assa; Neumann, Konstantin; Koenig, Paul-Albert; Prazeres da Costa, Clarissa; Vanes, Lesley; Kumar, Vinod; Johnson, Melissa; Menacho-Márquez, Mauricio ; Habermann, Bianca; Tybulewicz, Victor L.; Netea, Mihai; Bustelo, Xosé R. ; Ruland, Jürgen
Fecha de publicación2016
EditorElsevier
CitaciónCell Reports 17(10): 2572-2583 (2016)
ResumenFungal infections are major causes of morbidity and mortality, especially in immunocompromised individuals. The innate immune system senses fungal pathogens through Syk-coupled C-type lectin receptors (CLRs), which signal through the conserved immune adaptor Card9. Although Card9 is essential for antifungal defense, the mechanisms that couple CLR-proximal events to Card9 control are not well defined. Here, we identify Vav proteins as key activators of the Card9 pathway. Vav1, Vav2, and Vav3 cooperate downstream of Dectin-1, Dectin-2, and Mincle to engage Card9 for NF-κB control and proinflammatory gene transcription. Although Vav family members show functional redundancy, Vav1/2/3 mice phenocopy Card9 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.
Versión del editorhttps://doi.org/10.1016/j.celrep.2016.11.018
URIhttp://hdl.handle.net/10261/168774
Identificadoresdoi: 10.1016/j.celrep.2016.11.018
e-issn: 2211-1247
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