Dectin-1-induced RIPK1 and RIPK3 activation protects host against Candida albicans infection View Full Text


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Article Info

DATE

2019-04-03

AUTHORS

Mengtao Cao, Zhengxi Wu, Qi Lou, Wenli Lu, Jie Zhang, Qi Li, Yifan Zhang, Yikun Yao, Qun Zhao, Ming Li, Haibing Zhang, Youcun Qian

ABSTRACT

Necroptosis is a recently defined type of programmed cell death with the specific signaling cascade of receptor-interacting protein 1 (RIPK1) and RIPK3 complex to activate the executor MLKL. However, the pathophysiological roles of necroptosis are largely unexplored. Here, we report that fungus triggers myeloid cell necroptosis and this type of cell death contributes to host defense against the pathogen infection. Candida albicans as well as its sensor Dectin-1 activation strongly induced necroptosis in myeloid cells through the RIPK1-RIPK3-MLKL cascade. CARD9, a key adaptor in Dectin-1 signaling, was identified to bridge the RIPK1 and RIPK3 complex-mediated necroptosis pathway. RIPK1 and RIPK3 also potentiated Dectin-1-induced MLKL-independent inflammatory response. Both the MLKL-dependent and MLKL-independent pathways were required for host defense against C. albicans infection. Thus, our study demonstrates a new type of host defense system against fungal infection. More... »

PAGES

1-15

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41418-019-0323-8

    DOI

    http://dx.doi.org/10.1038/s41418-019-0323-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1113182219

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30944411


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