Journal
IMMUNOBIOLOGY
Volume 221, Issue 2, Pages 341-346Publisher
ELSEVIER GMBH
DOI: 10.1016/j.imbio.2015.10.001
Keywords
Neutrophils; NLRP12; Inflammation; Migration; TLR signalling
Categories
Funding
- Swiss National Science Foundation [SNF 310030-146187]
- National Health and Medical Research Council of Australia [490993, 1023297]
- University of Queensland Centennial Scholarship
- International Postgraduate Research Scholarship
- Natural Sciences and Engineering Research Council of Canada
- ANZ Trustee Medical Research Program postgraduate scholarship
- Ludwig Institute for Cancer Research
- Australian Research Council Future Fellowship [FT130100361]
- Queensland Smart Futures Fund
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NOD-like receptors (NLR) are a family of cytosolic pattern recognition receptors that include many key drivers of innate immune responses. NLRP12 is an emerging member of the NLR family that is closely related to the well-known inflammasome scaffold, NLRP3. Since its discovery, various functions have been proposed for NLRP12, including the positive regulation of dendritic cell (DC) and neutrophil migration and the inhibition of NF-kappa B and ERK signalling in DC and macrophages. We show here that NLRP12 is poorly expressed in murine macrophages and DC, but is strongly expressed in neutrophils. Using myeloid cells from WT and Nlrp12(-/-) mice, we show that, contrary to previous reports, NLRP12 does not suppress LPS- or infection-induced NF-kappa B or ERK activation in myeloid cells, and is not required for DC migration in vitro. Surprisingly, we found that Nlrp12 deficiency caused increased rather than decreased neutrophil migration towards the chemokine CXCL1 and the neutrophil parasite Leishmania major, revealing NLRP12 as a negative regulator of directed neutrophil migration under these conditions. (C) 2015 Elsevier GmbH. All rights reserved.
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