| pubmed-article:19144988 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19144988 | lifeskim:mentions | umls-concept:C0003315 | lld:lifeskim |
| pubmed-article:19144988 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:19144988 | lifeskim:mentions | umls-concept:C1956385 | lld:lifeskim |
| pubmed-article:19144988 | lifeskim:mentions | umls-concept:C0018133 | lld:lifeskim |
| pubmed-article:19144988 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:19144988 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:19144988 | pubmed:dateCreated | 2009-2-27 | lld:pubmed |
| pubmed-article:19144988 | pubmed:abstractText | Dendritic cells (DCs) can be classified into 2 distinct subsets: conventional DCs (cDCs) and plasmacytoid DCs (pDCs). cDCs can prime antigen-specific T-cell immunity, whereas in vivo function of pDCs as antigen-presenting cells remains controversial. We evaluated the contribution of pDCs to allogeneic T-cell responses in vivo in mouse models of graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation by an add-back study of MHC-expressing pDCs into major histocompatibility complex-deficient mice that were resistant to GVHD. Alloantigen expression on pDCs alone was sufficient to prime alloreactive T cells and cause GVHD. An inflammatory environment created by host irradiation has the decisive role in maturing pDCs for T-cell priming but this process does not require Toll-like receptor signaling. Thus, functional outcomes of pDC-T-cell interactions depend on the immunologic context of encounter. To our knowledge, these results are the first to directly demonstrate an in vivo pathogenic role of pDCs as antigen-presenting cells in an antigen-specific T cell-mediated disease in the absence of other DC subsets and to provide important insight into developing strategies for tolerance induction in transplantation. | lld:pubmed |
| pubmed-article:19144988 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19144988 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19144988 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19144988 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:19144988 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19144988 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:19144988 | pubmed:issn | 1528-0020 | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:HaradaMineM | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:NiiroHiroakiH | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:TeshimaTakano... | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:TanimotoMitsu... | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:AkashiKoichiK | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:AoyamaKazutos... | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:HashimotoDaig... | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:KarubeKennosu... | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:KoyamaMotokoM | lld:pubmed |
| pubmed-article:19144988 | pubmed:author | pubmed-author:MatsuokaKen-i... | lld:pubmed |
| pubmed-article:19144988 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19144988 | pubmed:day | 26 | lld:pubmed |
| pubmed-article:19144988 | pubmed:volume | 113 | lld:pubmed |
| pubmed-article:19144988 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19144988 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19144988 | pubmed:pagination | 2088-95 | lld:pubmed |
| pubmed-article:19144988 | pubmed:dateRevised | 2009-6-5 | lld:pubmed |
| pubmed-article:19144988 | pubmed:meshHeading | pubmed-meshheading:19144988... | lld:pubmed |
| pubmed-article:19144988 | pubmed:meshHeading | pubmed-meshheading:19144988... | lld:pubmed |
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| pubmed-article:19144988 | pubmed:meshHeading | pubmed-meshheading:19144988... | lld:pubmed |
| pubmed-article:19144988 | pubmed:meshHeading | pubmed-meshheading:19144988... | lld:pubmed |
| pubmed-article:19144988 | pubmed:meshHeading | pubmed-meshheading:19144988... | lld:pubmed |
| pubmed-article:19144988 | pubmed:meshHeading | pubmed-meshheading:19144988... | lld:pubmed |
| pubmed-article:19144988 | pubmed:meshHeading | pubmed-meshheading:19144988... | lld:pubmed |
| pubmed-article:19144988 | pubmed:meshHeading | pubmed-meshheading:19144988... | lld:pubmed |
| pubmed-article:19144988 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19144988 | pubmed:articleTitle | Plasmacytoid dendritic cells prime alloreactive T cells to mediate graft-versus-host disease as antigen-presenting cells. | lld:pubmed |
| pubmed-article:19144988 | pubmed:affiliation | Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Science, Fukuoka, Japan. | lld:pubmed |
| pubmed-article:19144988 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19144988 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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