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http://purl.uniprot.org/citations/29434592http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29434592http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29434592http://www.w3.org/2000/01/rdf-schema#comment"Signaling lymphocyte activation molecule family (SLAMF) receptors are essential regulators of innate and adaptive immune responses. The function of SLAMF5/CD84, a family member with almost ubiquitous expression within the hematopoietic lineage is poorly defined. In this article, we provide evidence that in human monocyte-derived dendritic cells (moDCs) SLAMF5 increases autophagy, a degradative pathway, which is highly active in dendritic cells (DCs) and plays a critical role in orchestration of the immune response. While investigating the underlying mechanism, we found that SLAMF5 inhibited proteolytic degradation of interferon regulatory factor 8 (IRF8) a master regulator of the autophagy process by a mechanism dependent on the E3-ubiquitin ligase tripartite motif-containing protein 21 (TRIM21). Furthermore, we demonstrate that SLAMF5 influences the ratio of CD1a+ cells in differentiating DCs and partakes in the regulation of IL-1β, IL-23, and IL-12 production in LPS/IFNγ-activated moDCs in a manner that is consistent with its effect on IRF8 stability. In summary, our experiments identified SLAMF5 as a novel cell surface receptor modulator of autophagy and revealed an unexpected link between the SLAMF and IRF8 signaling pathways, both implicated in multiple human pathologies."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.org/dc/terms/identifier"doi:10.3389/fimmu.2018.00062"xsd:string
http://purl.uniprot.org/citations/29434592http://purl.org/dc/terms/identifier"doi:10.3389/fimmu.2018.00062"xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Engel P."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Engel P."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Szabo A."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Szabo A."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Vereb G."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Vereb G."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Biro T."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Biro T."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Lanyi A."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Lanyi A."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Agod Z."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Agod Z."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Bacsi A."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Bacsi A."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Bencze D."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Bencze D."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Pazmandi K."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Pazmandi K."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Rajnavolgyi E."xsd:string
http://purl.uniprot.org/citations/29434592http://purl.uniprot.org/core/author"Rajnavolgyi E."xsd:string