Linked Life Data

21076058

Source:http://linkedlifedata.com/resource/pubmed/id/21076058

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-12-3
pubmed:abstractText
Th17 CD4 cells are critical to inflammation. Their secretion of IL-17 drives inflammation in human diseases, including inflammatory bowel disease. Differentiation of mature Th17 cells depends on stimulation with IL-6, TGF-?, and IL-21 and the induction of ROR?t, but IL-23 is essential to Th17 phenotype, stability, and function. Induction of Th17 cells can be antagonized by IL-4 or IFN-?, but mechanisms through which terminal differentiation can be inhibited have not been identified. Human IL-23R? (HuIL23R?)-chain mRNA transcripts exist that lack exon 9 ("?9"); these are translated to a truncated receptor containing the entire external domain. This soluble variant of the HuIL23R?-chain antagonizes Th17 maturation. It is secreted and present at low levels in the blood. It represents 10% of HuIL23R?-chain mRNA, binds IL-23 in solution, and inhibits the phosphorylation of STAT3 caused by IL-23. In in vitro Th17 cell differentiation experiments, ?9 inhibits the production of the Th17-associated cytokines IL-17A and IL-17F. ?9 does not bind IL-12; thus, it is a specific inhibitor of IL-23 and a modulator of Th17 cells. Our results indicate that this soluble form of HuIL23R? likely functions to regulate Th17 activity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
185
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7302-8
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
A naturally occurring, soluble antagonist of human IL-23 inhibits the development and in vitro function of human Th17 cells.
pubmed:affiliation
Genetic Immunology Laboratory, Humigen, The Institute for Genetic Immunology, Hamilton, NJ 08690, USA.
pubmed:publicationType
Journal Article