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SYK kinase signaling and the NLRP3 inflammasome in antifungal immunity

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Abstract

Host protection against fungi depends on intact innate and adaptive immune responses. Consistently, fungal infections can cause systemic life-threatening diseases in immunocomprimised individuals, suffering e.g. from cancer or AIDS. Recent work has uncovered essential roles for the spleen tyrosine kinase (SYK) and the cytosolic NLRP3 inflammasome for Interleukin-1β (IL-1β) production in innate antifungal immunity. Upon fungal infection, SYK is activated by several C-type lectin pattern recognition receptors on myeloid cells. Subsequently, SYK signals for the production of reactive oxygen species and for gene transcription to induce pro-inflammatory factors, including pro-IL-1β to initiate antifungal responses. Mature IL-1β production additionally requires cleavage of the pro-IL-1β precursor protein by the inflammatory caspase-1 which is controlled within the NLRP3 inflammasome. Here, we discuss how SYK signaling cooperates with the NLRP3 inflammasome for IL-1β production in antifungal immunity.

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Acknowledgements

Work in the authors’ laboratory is supported by a Max-Eder-Program grant from Deutsche Krebshilfe and SFB grants of the DFG to J.R. We thank Olaf Gross, Tobias Haas, and Konstanze Pechloff for critically reading the manuscript.

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The authors declare no competing financial interests.

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  1. III. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, 81675, Munich, Germany

    Hendrik Poeck & Jürgen Ruland

  2. Laboratory of Signaling in the Immune System, Helmholtz Zentrum München - German Research Center for Environmental Health, 85764, Neuherberg, Germany

    Jürgen Ruland

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Poeck, H., Ruland, J. SYK kinase signaling and the NLRP3 inflammasome in antifungal immunity. J Mol Med 88, 745–752 (2010). https://doi.org/10.1007/s00109-010-0631-4

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