| http://purl.uniprot.org/citations/22412192 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22412192 | http://www.w3.org/2000/01/rdf-schema#comment | "Nucleotide-binding oligomerization domain-like receptors (NLRs) are intracellular proteins involved in innate-driven inflammatory responses. The function of the family member NLR caspase recruitment domain containing protein 5 (NLRC5) remains a matter of debate, particularly with respect to NF-κB activation, type I IFN, and MHC I expression. To address the role of NLRC5, we generated Nlrc5-deficient mice (Nlrc5(Δ/Δ)). In this article we show that these animals exhibit slightly decreased CD8(+) T cell percentages, a phenotype compatible with deregulated MHC I expression. Of interest, NLRC5 ablation only mildly affected MHC I expression on APCs and, accordingly, Nlrc5(Δ/Δ) macrophages efficiently primed CD8(+) T cells. In contrast, NLRC5 deficiency dramatically impaired basal expression of MHC I in T, NKT, and NK lymphocytes. NLRC5 was sufficient to induce MHC I expression in a human lymphoid cell line, requiring both caspase recruitment and LRR domains. Moreover, endogenous NLRC5 localized to the nucleus and occupied the proximal promoter region of H-2 genes. Consistent with downregulated MHC I expression, the elimination of Nlrc5(Δ/Δ) lymphocytes by cytotoxic T cells was markedly reduced and, in addition, we observed low NLRC5 expression in several murine and human lymphoid-derived tumor cell lines. Hence, loss of NLRC5 expression represents an advantage for evading CD8(+) T cell-mediated elimination by downmodulation of MHC I levels-a mechanism that may be exploited by transformed cells. Our data show that NLRC5 acts as a key transcriptional regulator of MHC I in lymphocytes and support an essential role for NLRs in directing not only innate but also adaptive immune responses."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1102671"xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Braun M."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Schroder K."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Romero P."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Mattmann C."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Tschopp J."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Ferrero I."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Tardivel A."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Reith W."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Seguin-Estevez Q."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Guarda G."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Rebsamen M."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Heinz L.X."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Staehli F."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "MacDonald H.R."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/author | "Ludigs K."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/pages | "3820-3828"xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/title | "NLRC5 deficiency selectively impairs MHC class I- dependent lymphocyte killing by cytotoxic T cells."xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://purl.uniprot.org/core/volume | "188"xsd:string |
| http://purl.uniprot.org/citations/22412192 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22412192 |
| http://purl.uniprot.org/citations/22412192 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/22412192 |