Ignet

Gene Information

Gene symbol: NLRC4

Gene name: NLR family, CARD domain containing 4

HGNC ID: 16412

Synonyms: CLAN1, ipaf, CLANA, CLANB, CLANC, CLAND, CLR2.1, CLAN

Related Genes

#	Gene Symbol	Number of hits
1	AIM2	1 hits
2	CASP1	1 hits
3	CD4	1 hits
4	CD8A	1 hits
5	IL18	1 hits
6	IL1B	1 hits
7	IL33	1 hits
8	NAIP	1 hits
9	NLRP1	1 hits
10	NLRP3	1 hits
11	PYCARD	1 hits
12	TLR5	1 hits

Related Sentences

#	PMID	Sentence
1	18566365	We have recently shown that alum activates caspase-1 and induces secretion of mature IL-1beta and IL-18.
2	18566365	In this study we show that, in human and mouse macrophages, alum-induced secretion of IL-1beta, IL-18, and IL-33 is mediated by the NLR (nucleotide-binding domain leucine-rich repeat-containing) protein NLRP3 and its adaptor ASC, but not by NLRC4.
3	18624356	The Nlrp3 inflammasome is critical for aluminium hydroxide-mediated IL-1beta secretion but dispensable for adjuvant activity.
4	18624356	Alum has recently been shown to promote caspase-1 activation and IL-1beta secretion, but the cellular pathways involved remain elusive.
5	18624356	Here we report that the release of IL-1beta triggered by alum is abrogated in macrophages deficient in the NLR family, pyrin domain containing 3 (Nlrp3) protein and the apoptosis-associated speck-like protein containing a caspase recruitment domain (Asc) but not the NLR family, CARD domain containing 4 (Nlrc4) protein.
6	18624356	The requirement of the Nlrp3 inflammasome was specific for IL-1beta in that secretion of TNF-alpha was independent of Nlrp3 or Asc.
7	18624356	Consistently, processing of pro-caspase-1 induced by alum was abolished in macrophages lacking Nlrp3 or Asc.
8	18624356	Unlike caspase-1 processing and IL-1beta secretion triggered by LPS, alum-mediated activation of the inflammasome did not require exogenous ATP.
9	18624356	Importantly, induction of IgG production against human serum albumin by alum was unimpaired in mice deficient in Nlrp3.
10	18624356	These results indicate that alum induces IL-1beta via the Nlrp3 inflammasome but this activity is dispensable for alum-mediated adjuvant activity.
11	20533186	The recruitment of NLRs, namely IPAF, NAIPs and NALPs, by various potentially harmful stimuli leads to the assembly of inflammasomes, multimeric caspase-activating complexes entailing the sensor NLR, intracellular adaptor proteins, and procaspase-1 and -5.
12	20533186	The caspase activation is necessarily required for the processing and secretion of proinflammatory cytokines, such as interleukin (IL)-1b, IL-18, and IL-33.
13	21072873	TLR5 or NLRC4 is necessary and sufficient for promotion of humoral immunity by flagellin.
14	21072873	Thus, we examined the ability of flagellin to induce cytokines and elicit/promote murine antibody responses upon deletion of the flagellin receptors TLR5 and/or NLRC4 (also referred to as IPAF) using a prime/boost regimen.
15	21072873	In TLR5-KO mice, flagellin failed to induce NF-κB-regulated cytokines such as keratinocyte-derived chemokine (CXCL1) but induced WT levels of the inflammasome cytokine IL-18 (IL-1F4).
16	21072873	TLR5 or NLRC4 is necessary and sufficient for promotion of humoral immunity by flagellin.
17	21072873	Thus, we examined the ability of flagellin to induce cytokines and elicit/promote murine antibody responses upon deletion of the flagellin receptors TLR5 and/or NLRC4 (also referred to as IPAF) using a prime/boost regimen.
18	21072873	In TLR5-KO mice, flagellin failed to induce NF-κB-regulated cytokines such as keratinocyte-derived chemokine (CXCL1) but induced WT levels of the inflammasome cytokine IL-18 (IL-1F4).
19	21538346	The immunostimulatory properties conferred by vaccine adjuvants require caspase-1 for processing of IL-1β and IL-18.
20	21538346	Listeria monocytogenes is detected in the cytosol by the NLRC4, NLRP3 and AIM2 inflammasomes.
21	21538346	This strain hyperactivated caspase-1 and was preferentially cleared via NLRC4 detection in an IL-1β/IL-18 independent manner.
22	22323829	Here, we show that expression of the TLR ligand flagellin within tumor cells constitutes an effective antitumor vaccination strategy that relies on simultaneous engagement of TLR5 and the Nod-like receptors (NLRs) NLRC4/NAIP5 (neuronal apoptosis inhibitory protein 5) by flagellin along with associative recognition of tumor antigen for optimal antigen presentation to T cells.
23	22323829	Although TLR5 signaling was critical for mediating rapid macrophage-dependent clearance of flagellin-expressing tumor cells in vivo, TLR5 and NLRC4/NAIP5 were equally important for priming antitumor CD4(+) and CD8(+) T cells and suppressing tumor growth.
24	22323829	Vaccination with irradiated flagellin-expressing tumor cells prevented tumor development, and disrupting flagellin recognition by TLR5 or NLRC4/NAIP5 impaired protective immunization against an existing or subsequent tumor.
25	22323829	Here, we show that expression of the TLR ligand flagellin within tumor cells constitutes an effective antitumor vaccination strategy that relies on simultaneous engagement of TLR5 and the Nod-like receptors (NLRs) NLRC4/NAIP5 (neuronal apoptosis inhibitory protein 5) by flagellin along with associative recognition of tumor antigen for optimal antigen presentation to T cells.
26	22323829	Although TLR5 signaling was critical for mediating rapid macrophage-dependent clearance of flagellin-expressing tumor cells in vivo, TLR5 and NLRC4/NAIP5 were equally important for priming antitumor CD4(+) and CD8(+) T cells and suppressing tumor growth.
27	22323829	Vaccination with irradiated flagellin-expressing tumor cells prevented tumor development, and disrupting flagellin recognition by TLR5 or NLRC4/NAIP5 impaired protective immunization against an existing or subsequent tumor.
28	22323829	Here, we show that expression of the TLR ligand flagellin within tumor cells constitutes an effective antitumor vaccination strategy that relies on simultaneous engagement of TLR5 and the Nod-like receptors (NLRs) NLRC4/NAIP5 (neuronal apoptosis inhibitory protein 5) by flagellin along with associative recognition of tumor antigen for optimal antigen presentation to T cells.
29	22323829	Although TLR5 signaling was critical for mediating rapid macrophage-dependent clearance of flagellin-expressing tumor cells in vivo, TLR5 and NLRC4/NAIP5 were equally important for priming antitumor CD4(+) and CD8(+) T cells and suppressing tumor growth.
30	22323829	Vaccination with irradiated flagellin-expressing tumor cells prevented tumor development, and disrupting flagellin recognition by TLR5 or NLRC4/NAIP5 impaired protective immunization against an existing or subsequent tumor.
31	24276957	Receptors of the innate immune system including Toll like receptor 5, ICE protease activating factor, and neuronal apoptosis inhibitory protein 5 signal in response to bacterial flagellins.
32	24637756	Upon bacterial invasion into a host, flagellin functions as a pathogen-associated molecular pattern that is recognized by immune receptors, such as Toll-like receptor 5 (TLR5) and NAIP5/NLRC4, and activates host innate immunity against pathogens.
33	24637756	Future structure-based functional studies of paflagellin would extend the knowledge of the TLR5 or NAIP5/NLRC4 activation mechanisms of flagellin and would make a significant contribution to the design of flagellin vaccines and antiradiation therapeutics.
34	24637756	Upon bacterial invasion into a host, flagellin functions as a pathogen-associated molecular pattern that is recognized by immune receptors, such as Toll-like receptor 5 (TLR5) and NAIP5/NLRC4, and activates host innate immunity against pathogens.
35	24637756	Future structure-based functional studies of paflagellin would extend the knowledge of the TLR5 or NAIP5/NLRC4 activation mechanisms of flagellin and would make a significant contribution to the design of flagellin vaccines and antiradiation therapeutics.
36	25531528	Flagellin is a bacterial protein that stimulates the innate immune response via binding to extracellular Toll-like receptor 5 (TLR5) and also via interaction with intracellular NOD-like receptor C4 (NLRC4), leading to production of pro-inflammatory cytokines.
37	25786687	Cholera toxin, and the related nontoxic adjuvants mmCT and dmLT, promote human Th17 responses via cyclic AMP-protein kinase A and inflammasome-dependent IL-1 signaling.
38	25786687	CT, mmCT, and dmLT strongly enhanced IL-17A and to a lesser extent IL-13 responses, but had little effect on IFN-γ production or cell proliferation.
39	25786687	Intracellular cytokine staining revealed that the enhanced IL-17A production was largely confined to CD4(+) T cells and coculture experiments showed that the IL-17A promotion was effectively induced by adjuvant-treated monocytes.
40	25786687	Thus, inhibition of cAMP-dependent protein kinase A was abolished, and stimulation with a cAMP analog mimicked the adjuvant effect.
41	25786687	Furthermore, CT, mmCT, and dmLT induced IL-1β production and caspase-1 activation in monocytes, which was associated with increased expression of key proinflammatory and inflammasome-related genes, including NLRP1, NLRP3, and NLRC4.
42	25786687	Inflammasome inhibition with a specific caspase-1 inhibitor, or blocking of IL-1 signaling by IL-1 receptor antagonist, abrogated the Th17-promoting effect.
43	25786687	We conclude that CT, mmCT, and dmLT promote human Th17 responses via cAMP-dependent protein kinase A and caspase-1/inflammasome-dependent IL-1 signaling.