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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2011-10-3
pubmed:abstractText
Pattern recognition receptors (PRRs) constitute the first line of host defense against bacterial, fungal and viral pathogens. Upon sensing microbial infection, PRRs initiate a cascade of signal transduction and transcriptional events to induce the production of inflammatory cytokines. As a result, many pathogens have evolved to evade PRR detection and activation in order to establish a successful infection. In a recent report, we described how a viral protein named Orf63 encoded by Kaposi's sarcoma-associated herpesvirus (KSHV) inhibits activation of several members of a family of PRRs called NLRs (nucleotide-binding and oligomerization, leucine-rich repeat) by functionally inhibiting the NLR response. This resulted in reduced NLR-dependent pro-inflammatory cytokine secretion and cell death. Moreover, Orf63 was essential in the KSHV lifecycle. Thus, our work suggests KSHV has evolved to encode a functional homolog of NLR proteins in an effort to suppress the host inflammatory response.
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:month
Jul
pubmed:issn
1942-0889
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
416-8
pubmed:year
2011
pubmed:articleTitle
Inhibition of the inflammasome response by a viral protein that interacts with NLRs.
pubmed:affiliation
Lineberger Comprehensive Cancer Center and Department of Microbiology & Immunology; University of North Carolina; Chapel Hill, NC USA.
pubmed:publicationType
Journal Article