Source:http://linkedlifedata.com/resource/pubmed/id/18586982
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
2008-10-1
|
pubmed:abstractText |
IL-17-producing Th cells (Th17) are a distinct subset of effector cells that bridge the innate and adaptive immune system and are implicated in autoimmune disease processes. CD4(+) splenocytes from DO11.10 mice were activated with OVA peptide(323-339) and maintained under Th17 polarization conditions, resulting in significantly higher proportions of IL-17(+) T cells compared with nonpolarized (Th0) cells. Th17-polarizing conditions significantly increased the proportion of cells expressing the chemokine receptors CCR2, CCR6, and CCR9 when compared with Th0 cells. In contrast, there was a significant decrease in the proportion of cells expressing CXCR3 under Th17-polarizing conditions compared with nonpolarizing conditions. The respective chemokine agonists for CCR2 (CCL2 and CCL12), CCR6 (CCL20), and CCR9 (CCL25) elicited migration and PI-3K-dependent signaling events in Th17-polarized cells, thus indicating that all three receptors were functionally and biochemically responsive. Furthermore, postmigration phenotypic analysis demonstrated that the agonists for CCR2 and CCR6, but not CCR9, stimulated a modest enrichment of IL-17(+) cells compared with the premigration population. Pan-isoform inhibitors of PI-3K/Akt signaling prevented CCR2- and CCR6-mediated, polarized Th17 cell migration in a concentration-dependent manner. The unique chemokine receptor expression pattern of Th17 cells and their corresponding PI-3K-dependent migratory responses are important for understanding the pathogenesis of autoimmune diseases and may provide opportunities for the application of CCR2 and CCR6 antagonists and PI-3K isoform-selective inhibitors in defined inflammatory settings.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCR6 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ccr2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR6,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0741-5400
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
84
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1202-12
|
pubmed:dateRevised |
2010-11-18
|
pubmed:meshHeading |
pubmed-meshheading:18586982-Animals,
pubmed-meshheading:18586982-CD4-Positive T-Lymphocytes,
pubmed-meshheading:18586982-Cell Movement,
pubmed-meshheading:18586982-Cell Separation,
pubmed-meshheading:18586982-Cytokines,
pubmed-meshheading:18586982-Gene Expression Profiling,
pubmed-meshheading:18586982-Gene Expression Regulation,
pubmed-meshheading:18586982-Mice,
pubmed-meshheading:18586982-Mice, Inbred BALB C,
pubmed-meshheading:18586982-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:18586982-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:18586982-Receptors, CCR2,
pubmed-meshheading:18586982-Receptors, CCR6,
pubmed-meshheading:18586982-Receptors, Chemokine,
pubmed-meshheading:18586982-Spleen,
pubmed-meshheading:18586982-T-Lymphocytes, Helper-Inducer
|
pubmed:year |
2008
|
pubmed:articleTitle |
Evidence for PI-3K-dependent migration of Th17-polarized cells in response to CCR2 and CCR6 agonists.
|
pubmed:affiliation |
Department of Pharmacy and Pharmacology, University of Bath, Claverton Down, Bath, BA2 7AY, UK.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|