Source:http://linkedlifedata.com/resource/pubmed/id/15780988
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2005-3-22
|
| pubmed:abstractText |
The class IV semaphorin Sema4A provides a costimulatory signal to T cells. To investigate the possible developmental and regulatory roles of Sema4A in vivo, we generated Sema4A-deficient mice. Although Sema4A-deficient mice develop normally, DCs and T cells from knockout mice display poor allostimulatory activities and T helper cell (Th) differentiation, respectively. Interestingly, in addition to its expression on DCs, Sema4A is upregulated on Th1-differentiating cells, and it is necessary for in vitro Th1 differentiation and T-bet expression. Consequently, in vivo antigen-specific T cell priming and antibody responses against T cell-dependent antigens are impaired in the mutant mice. Additionally, Sema4A-deficient mice exhibit defective Th1 responses. Furthermore, reconstitution studies with antigen-pulsed DCs reveal that DC-derived Sema4A is important for T cell priming, while T cell-derived Sema4A is involved in developing Th1 responses. Collectively, these results indicate a nonredundant role of Sema4A not only in T cell priming, but also in the regulation of Th1/Th2 responses.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
1074-7613
|
| pubmed:author |
pubmed-author:AkiraShizuoS,
pubmed-author:IshidaIsaoI,
pubmed-author:KashiwamuraShin-IchiroS,
pubmed-author:KikutaniHitoshiH,
pubmed-author:Ko-MitamuraElizabeth PEP,
pubmed-author:KumanogohAtsushiA,
pubmed-author:MarukawaSatokoS,
pubmed-author:MizuiMasayukiM,
pubmed-author:MorishitaHiroshiH,
pubmed-author:OkabeMasaruM,
pubmed-author:PrasadDurbaka V RDV,
pubmed-author:ShikinaTakashiT,
pubmed-author:SuzukiKazuhiroK,
pubmed-author:TakamatsuHyotaH,
pubmed-author:TakedaKiyoshiK,
pubmed-author:TakegaharaNorikoN,
pubmed-author:TamuraManabuM,
pubmed-author:ToyofukuToshihikoT,
pubmed-author:TsutsuiHirokoH,
pubmed-author:UematsuSatoshiS,
pubmed-author:YamamotoMidoriM,
pubmed-author:YukawaKazunoriK
|
| pubmed:issnType |
Print
|
| pubmed:volume |
22
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
305-16
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:15780988-Animals,
pubmed-meshheading:15780988-Cell Differentiation,
pubmed-meshheading:15780988-Dendritic Cells,
pubmed-meshheading:15780988-Flow Cytometry,
pubmed-meshheading:15780988-Gene Targeting,
pubmed-meshheading:15780988-Lymphocyte Activation,
pubmed-meshheading:15780988-Mice,
pubmed-meshheading:15780988-Mice, Knockout,
pubmed-meshheading:15780988-Semaphorins,
pubmed-meshheading:15780988-T-Lymphocytes
|
| pubmed:year |
2005
|
| pubmed:articleTitle |
Nonredundant roles of Sema4A in the immune system: defective T cell priming and Th1/Th2 regulation in Sema4A-deficient mice.
|
| pubmed:affiliation |
Department of Molecular Immunology and CREST Program of JST, Research Institute for Microbial DiseasesOsaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|