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. 2009 Dec 15;183(12):8061-7.
doi: 10.4049/jimmunol.0902477.

Involvement of the NLRP3 inflammasome in innate and humoral adaptive immune responses to fungal beta-glucan

Himanshu Kumar  1 , Yutaro Kumagai, Tetsuo Tsuchida, Paul A Koenig, Takashi Satoh, Zijin Guo, Myoung Ho Jang, Tatsuya Saitoh, Shizuo Akira, Taro Kawai
Affiliations

Involvement of the NLRP3 inflammasome in innate and humoral adaptive immune responses to fungal beta-glucan

Himanshu Kumar et al. J Immunol. .

Abstract

Fungal beta-glucan, such as curdlan, triggers antifungal innate immune responses as well as shaping adaptive immune responses. In this study, we identified a key pathway that couples curdlan to immune responses. Curdlan promoted the production of the proinflammatory cytokine IL-1beta by dendritic cells and macrophages through the NLRP3 inflammasome. Stimulation with Candida albicans and Saccharomyces cerevisiae also triggered the NLRP3 inflammasome-mediated IL-1beta production. In vivo, NLRP3 was required for efficient Ag-specific Ab production when curdlan was used as an adjuvant, whereas it was dispensable for the induction of Th1 and Th17 cell differentiation. Furthermore, stimulation of purified B cells with curdlan-induced CD69 up-regulation and IgM production while stimulation with other NLRP3 inflammasome activators, such as silica and aluminum salt, did not. Notably, this induction required NLRP3 but was independent of Toll-like receptor and IL-1 receptor family signaling, suggesting the presence of NLRP3-dependent and IL-1 receptor family independent mechanisms in B cells responsible for Ab responses. Collectively, these findings reveal a critical role for the NLRP3 inflammasome in the regulation of antifungal innate immune responses as well as B cell activation.

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