Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7357
pubmed:dateCreated
2011-7-28
pubmed:abstractText
Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1476-4687
pubmed:author
pubmed:issnType
Electronic
pubmed:day
28
pubmed:volume
475
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
514-8
pubmed:dateRevised
2011-10-4
pubmed:meshHeading
pubmed-meshheading:21765430-Animals, pubmed-meshheading:21765430-Antibodies, pubmed-meshheading:21765430-Antigens, CD3, pubmed-meshheading:21765430-CD4-Positive T-Lymphocytes, pubmed-meshheading:21765430-Cell Movement, pubmed-meshheading:21765430-Chemokine CCL20, pubmed-meshheading:21765430-Disease Models, Animal, pubmed-meshheading:21765430-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:21765430-Female, pubmed-meshheading:21765430-Gene Expression Profiling, pubmed-meshheading:21765430-Gene Expression Regulation, pubmed-meshheading:21765430-Influenza A virus, pubmed-meshheading:21765430-Interleukin-17, pubmed-meshheading:21765430-Intestine, Small, pubmed-meshheading:21765430-Male, pubmed-meshheading:21765430-Mice, pubmed-meshheading:21765430-Mice, Inbred BALB C, pubmed-meshheading:21765430-Mice, Inbred C57BL, pubmed-meshheading:21765430-Mice, Transgenic, pubmed-meshheading:21765430-Orthomyxoviridae Infections, pubmed-meshheading:21765430-Receptors, CCR6, pubmed-meshheading:21765430-Sepsis, pubmed-meshheading:21765430-Staphylococcal Infections, pubmed-meshheading:21765430-Th17 Cells
pubmed:year
2011
pubmed:articleTitle
Control of TH17 cells occurs in the small intestine.
pubmed:affiliation
Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. enric.esplugues@yale.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural