Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-11-8
pubmed:abstractText
Macrophages play key roles in inflammation. During the onset of the inflammatory process, these phagocytic cells become activated and have destructive effects. Macrophage activation, which involves the induction of more than 400 genes, results in an increased capacity to eliminate bacteria and to regulate many other cells through the release of cytokines and chemokines. However, excessive activation has damaging effects, such as septic shock, which can lead to multiple organ dysfunction syndrome and death. In other situations, persistence of proinflammatory activity results in the development of chronic inflammation, such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease. To prevent undesirable effects, several mechanisms have evolved to control the excess of activation, thereby leading to macrophage deactivation and the resolution of inflammation. In this review, we discuss several mechanisms that mediate macrophage deactivation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1557-8445
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
108
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-20
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Macrophage proinflammatory activation and deactivation: a question of balance.
pubmed:affiliation
Nuclear Receptors Group, Department of Physiology, School of Biology, Barcelona, Spain.
pubmed:publicationType
Journal Article, Review