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