| pubmed-article:15808537 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15808537 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:15808537 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:15808537 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:15808537 | lifeskim:mentions | umls-concept:C1413694 | lld:lifeskim |
| pubmed-article:15808537 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:15808537 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:15808537 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:15808537 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:15808537 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15808537 | pubmed:dateCreated | 2005-4-5 | lld:pubmed |
| pubmed-article:15808537 | pubmed:abstractText | Antibodies can mediate injury of organ transplants by several mechanisms, including complement activation and interaction with Fc receptors on cells. We tested the hypothesis that antibodies could also cause up-regulation of complement receptors on cells to increase the responses to complement activation by interaction with split products of C3. In our experimental model, B10.A (H-2(a)) cardiac transplants survive significantly longer in C57BL/6 (H-2(b)) immunoglobulin knockout recipients (IgKO) than in their wild-type counterparts. Passive transfer of specific antibodies to donor MHC class I to IgKO recipients of cardiac allografts at the time coinciding with a vigorous cellular infiltration reconstituted acute rejection. We tested the effects of alloantibodies on CR1/2 expression by alloantigen-stimulated T cells. Both CD4(+)/CR1/2(+) and CD8(+)/CR1/2(+) populations of T cells were expanded in C57BL/6 splenocytes stimulated by B10.A alloantigen in 7-day MLR after coculture with endothelial cells sensitized with IgG1 and IgG2b mAb specific to MHC. Endothelial cells sensitized with antibodies also caused an expansion of CD8(+) T cells expressing CR1/2 in lymph node lymphocytes harvested from a C57BL/6 recipient of a B10.A cardiac allograft. These data suggest that antibodies can augment the cellular rejection process through expanding the population of T cells interacting with complement split products. | lld:pubmed |
| pubmed-article:15808537 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15808537 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15808537 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15808537 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15808537 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15808537 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15808537 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15808537 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15808537 | pubmed:issn | 0041-1345 | lld:pubmed |
| pubmed-article:15808537 | pubmed:author | pubmed-author:BaldwinW... | lld:pubmed |
| pubmed-article:15808537 | pubmed:author | pubmed-author:QianZZ | lld:pubmed |
| pubmed-article:15808537 | pubmed:author | pubmed-author:WasowskaB ABA | lld:pubmed |
| pubmed-article:15808537 | pubmed:author | pubmed-author:BielerJ GJG | lld:pubmed |
| pubmed-article:15808537 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15808537 | pubmed:volume | 37 | lld:pubmed |
| pubmed-article:15808537 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15808537 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15808537 | pubmed:pagination | 32-4 | lld:pubmed |
| pubmed-article:15808537 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:meshHeading | pubmed-meshheading:15808537... | lld:pubmed |
| pubmed-article:15808537 | pubmed:articleTitle | Expression of CR1/2 receptor on alloantigen-stimulated mouse T cells. | lld:pubmed |
| pubmed-article:15808537 | pubmed:affiliation | Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. | lld:pubmed |
| pubmed-article:15808537 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15808537 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15808537 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:15808537 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:12902 | entrezgene:pubmed | pubmed-article:15808537 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:15808537 | lld:entrezgene |
