Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-7-3
pubmed:abstractText
Nuclear macromolecules, in addition to their intracellular role in regulating cell function, can translocate into the extracellular space where they can activate innate immunity. This translocation can occur in various settings and reflects the dynamic nature of nuclear structure. Of nuclear molecules, DNA and the DNA-binding protein, HMGB1, display distinct patterns of immune activity. For DNA, immune activity depends on sequence, base methylation, and context. While bacterial DNA is an immune activator, mammalian DNA is either inert or inhibitory when free. In contrast, mammalian DNA in the form of immune complexes can trigger immune cell activation. As shown in in vivo and in vitro studies, DNA can exit cells during apoptotic as well as necrotic cell death in a process that may depend on the presence of macrophages. Like DNA, HMGB1 can exit cells and acquire immune properties. For HMGB1, the translocation occurs in macrophages that have been stimulated by Toll-like receptor (TLR) ligands as well as cytokines; HMGB1 release can also occur with apoptotic as well as necrotic death. While HMGB1 alone can display cytokine activity, it may also activate cells in conjunction with other immune stimulators such as TLR ligands. For both DNA and HMGB1, the immune properties may therefore reflect the array of other endogenous as well as exogenous molecules present.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1546-3222
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
258-62
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
The role of nuclear macromolecules in innate immunity.
pubmed:affiliation
Durham VA Medical Center and Duke University Medical Center, Box 151G, 508 Fulton St., Durham, NC 27705, USA. dpiset@acpub.duke.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't