Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2007-8-31
pubmed:abstractText
Dendritic cells (DCs) are powerful sensors of foreign pathogens as well as cancer cells and provide the first line of defence against infection. They also serve as a major link between innate and adaptive immunity. Immature DCs respond to incoming danger signals and undergo maturation to produce high levels of proinflammatory cytokines including type I interferons (IFNs) to establish innate immunity. They then present antigens to T lymphocytes to stimulate lasting specific immune responses. Recent studies point to the importance of DCs in the induction of peripheral tolerance. Transcription factors of the IRF family have emerged as crucial controllers of many aspects of DC activity, playing an essential role in the establishment of early innate immunity. Furthermore, eight of the nine members of the IRF family have been shown to control either the differentiation and/or the functional activities of DCs. In this review, we focus on three aspects of DC properties that are under the control of IRFs: (1) the development and differentiation, (2) maturation in response to toll-like receptor (TLR) signalling and the production of anti-microbial cytokines, and (3) activation and expansion of lymphocytes to generate protective or tolerogenic immune responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1359-6101
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
503-10
pubmed:meshHeading
pubmed:articleTitle
The role of the interferon regulatory factor (IRF) family in dendritic cell development and function.
pubmed:affiliation
Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Roma, Italy. lucia.gabriele@iss.it
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Intramural