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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)

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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

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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-1beta (IL-1beta) 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-1beta to initiate antifungal responses. Mature IL-1beta production additionally requires cleavage of the pro-IL-1beta 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-1beta production in antifungal immunity.

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