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Immunobiology. 2016 Feb;221(2):341-6. doi: 10.1016/j.imbio.2015.10.001. Epub 2015 Oct 23.

NLRP12 is a neutrophil-specific, negative regulator of in vitro cell migration but does not modulate LPS- or infection-induced NF-κB or ERK signalling.

Author information

1
Institute for Molecular Bioscience, University of Queensland, St Lucia 4072, Australia.
2
Institut für Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, and TUM Graduate School, Technische Universität München, 81675 Munich, Germany.
3
Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland; WHO-Immunology Research and Training Centre, University of Lausanne, CH-1066 Epalinges, Switzerland.
4
Ludwig Center for Cancer Research, University of Lausanne, CH-1066 Epalinges, Switzerland.
5
Institute for Molecular Bioscience, University of Queensland, St Lucia 4072, Australia. Electronic address: K.Schroder@imb.uq.edu.au.

Abstract

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-κB 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-κB 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.

KEYWORDS:

Inflammation; Migration; NLRP12; Neutrophils; TLR signalling

PMID:
26514298
DOI:
10.1016/j.imbio.2015.10.001
[Indexed for MEDLINE]

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