Nlrp10

NLRPs (acronym for "NIGHT, LRR and PYD domains-containing protein) are, together with the NOD1 and NOD2 proteins, members of the NLR (Nod-like Receptor) protein family and play a major role in innate immunity as pathogen recognition receptors (PPRs). Like the NOD proteins, NLRPs are expressed exclusively cytoplasmically. All NLRPs (they all contain a pyrin domain) are encoded by a common gene family in humans. NLRPs are characterised by their ability to activate different inflammatory complexes.

NLRP10 is a cytosolic protein encoded in humans by the NLRP10 gene located on chromosome 11p15.4 (Location: Chr 11: 7.96 - 7.97 Mb) within a cluster of other NLRP genes.

Inflammasomes are differently composed cytosolic protein complexes, whereby the different NLRPs are of great importance for their functionality. Inflammasomes are predominantly found in immune cells such as dendritic cells and macrophages.

The activation of an inflammasome complex leads to the expression of different caspases, which convert inactive interleukin-1beta and interleukin-18 into their active form.

Most short NLRPs have an N-terminal pyrin domain (PYD), followed by the NIGHT domain, a NIGHT-associated domain (NAD), and a C-terminal leucine-rich region (LRR). In NLRP10, the LRR region is missing.

Little is known about the functions and mode of action of NLRP10.

NLRP10 has a regulatory function in the innate and adaptive immune system. Thus, this pathogen recognition receptor plays an essential role in the homeostasis and immune function of the intestine. NLRP10 is increasingly expressed after stimulation by lipopolysaccharides (Damm A et al 2016).

NLRP10 is expressed in keratinocytes. Thus, this NLRP in the epidermis has an essential function in the defence against invasive bacteria.

NLRP10 deficient mice do not show any healing disorders in experimental wounds. However, the cutaneous inflammatory response was significantly reduced in contact allergic eczema, with a reduced number of CD4+/CD8+ cells.

NLRP10 deficient mice showed a high propensity for Candida albicans infections. These mouse strains produced IL-1b at normal levels, but did not show any loss of their phagocytotic abilities. However, NLRP10 was shown to be essential for the Th1/Th17 lymphocyte-triggered Candida-specific immune response (Joly S et al. 2012).

1. Castaño-Rodríguez N et al (2014) The NOD-like receptor signalling pathway in Helicobacter pylori infection and related gastric cancer: a case-control study and gene expression analyses. PLoS One 9:e98899.
2. Chu JQ et al (2016) Production of IL-1β and Inflammasome with Up-Regulated Expressions of NOD-Like Receptor Related Genes in Toxoplasma gondii-Infected THP-1 Macrophages. Korean J Parasitol 54:711-717.
3. Joly S et al (2012) Cutting edge: Nlrp10 is essential for protective antifungal adaptive immunity against Candida albicans. J. immune 189: 4713-4717
4. Ponsuksili S et al (2006) Bovine NALP5, NALP8, and NALP9 genes: assignment to a QTL region and the expression in adult tissues, oocytes, and preimplantation embryos. Biol Reprod 74:577-584.