Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-7-27
pubmed:abstractText
Th cells that produce IL-17 (Th17 cells) are a distinct subset of Th cells implicated in several autoimmune diseases. Although CD28-B7 interaction has been shown to be involved in Th17 differentiation in vitro, the role of CTLA-4 in controlling Th17 development is completely unknown. We report in this paper that blocking the CTLA-4-B7 interaction potentiates Th17 cell differentiation in vitro and in vivo. Furthermore, blocking CTLA-4-B7 interaction in vivo confers the susceptibility of experimental autoimmune myocarditis to CD28(-/-) mice or increases the severity of experimental autoimmune myocarditis in wild-type mice. The enhanced disease susceptibility is mediated by heightened Th17 responses. With these results, we are the first to demonstrate that CTLA-4-B7 interaction inhibits Th17 differentiation in vitro and in vivo and suppresses Th17-mediated autoimmunity.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-10903737, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-11244036, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-12087419, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-12368911, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-14575153, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-15585834, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-16200068, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-16880257, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-17227914, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-17375096, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-18250481, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-18779348, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-19132915, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-7481803, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-7584144, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-8228811, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-8676074, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-9143690, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-9430233, http://linkedlifedata.com/resource/pubmed/commentcorrection/20601598-9892625
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
185
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1375-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:20601598-Amino Acid Sequence, pubmed-meshheading:20601598-Animals, pubmed-meshheading:20601598-Antigens, CD, pubmed-meshheading:20601598-Antigens, CD28, pubmed-meshheading:20601598-Antigens, CD80, pubmed-meshheading:20601598-Autoimmune Diseases, pubmed-meshheading:20601598-CTLA-4 Antigen, pubmed-meshheading:20601598-Cell Differentiation, pubmed-meshheading:20601598-Cells, Cultured, pubmed-meshheading:20601598-Down-Regulation, pubmed-meshheading:20601598-Genetic Predisposition to Disease, pubmed-meshheading:20601598-Growth Inhibitors, pubmed-meshheading:20601598-Interleukin-17, pubmed-meshheading:20601598-Mice, pubmed-meshheading:20601598-Mice, Inbred BALB C, pubmed-meshheading:20601598-Mice, Inbred C57BL, pubmed-meshheading:20601598-Mice, Knockout, pubmed-meshheading:20601598-Molecular Sequence Data, pubmed-meshheading:20601598-Myocarditis, pubmed-meshheading:20601598-T-Lymphocytes, Helper-Inducer
pubmed:year
2010
pubmed:articleTitle
Cutting edge: CTLA-4--B7 interaction suppresses Th17 cell differentiation.
pubmed:affiliation
Laboratory of Molecular Cancer Biology, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural