Linked Life Data

16620015

Source:http://linkedlifedata.com/resource/pubmed/id/16620015

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-4-19
pubmed:abstractText
In conclusion, during inflammation, DCs are likely activated by inflammatory signals and induced to migrate to T cell zones of organized lymphoid tissues where the cells induce T cell responses. In addition to their established role in T cell priming and the induction of tolerance, DCs may act to enhance (or possibly suppress) T cell responses at sites of mucosal inflammation. Determining the importance of DCs in this regard, as well as establishing a potential role for DCs in continuous activation of naive or central memory cells in lymph nodes draining inflammatory sites, will elucidate the role of DCs as a potential therapeutic target for chronic inflammatory diseases, like IBD. Resident intestinal macrophages are noninflammatory and do not efficiently present antigens to intestinal T cells, yet are avidly phagocytic and able to kill internalized organisms. During intestinal inflammation, monocytes are recruited from the blood, become inflammatory macrophages in the inflamed tissue, and are major contributors to tissue destruction and perpetuation of inflammation via their production of chemokines and pro-inflammatory cytokines. Macrophages may also contribute directly to DC activation and maturation, which would drive DCs to present antigens from the bacterial flora to T cells locally within tissue or to more efficiently traffic to T cell zones of lymphoid tissue. Thus, DCs and macrophages have evolved functional niches that promote cooperation in the prevention of untoward intestinal inflammation in the steady state and in the eradication of invasive microorganisms during infection. The balance between suppressing inflammation and promoting host defense is altered in humans with IBD allowing a persistent inflammatory response to commensal bacteria. Based on studies from animal models, the pathogenesis of IBD likely involves either the lack of appropriate regulation from T cells, or an over-production of effector T cells. The end result of these potential mechanisms is the abnormal induction and/or survival of effector T cells and the production of factors such as cytokines by inflammatory macrophages and neutrophils that result in tissue destruction. The destructive process likely involves normally tolerizing DCs, which in the microenvironment of the inflamed mucosa activate T cell responses to normal flora in both draining lymphoid tissues and at sites of inflammation, with macrophages and neutrophils contributing the bulk of inflammatory and destructive cytokines.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0065-2598
pubmed:author
pubmed:issnType
Print
pubmed:volume
579
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
117-32
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Involvement of dendritic cells in the pathogenesis of inflammatory bowel disease.
pubmed:affiliation
Laboratory of Molecular Immunology, NIAID, National Institutes of Health, Bethesda, MD, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, N.I.H., Extramural