| pubmed-article:11342443 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11342443 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:11342443 | lifeskim:mentions | umls-concept:C0014792 | lld:lifeskim |
| pubmed-article:11342443 | lifeskim:mentions | umls-concept:C0229664 | lld:lifeskim |
| pubmed-article:11342443 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:11342443 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:11342443 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:11342443 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:11342443 | pubmed:dateCreated | 2001-5-8 | lld:pubmed |
| pubmed-article:11342443 | pubmed:abstractText | Red blood cells (RBCs) are known to perform one prominent function: to carry and deliver oxygen to the tissues. Earlier studies, however, suggested a role for RBCs in potentiating T-cell proliferation in vitro. Here it is shown that the presence of RBCs in cultures of stimulated human peripheral blood lymphocytes strengthens T-cell proliferation and survival. Analysis of phosphatidylserine externalization and DNA fragmentation showed that RBCs inhibit T-cell apoptosis. This inhibition correlated with a reduction in CD71 but not CD95 expression. RBCs enhanced T-cell proliferation and survival upon activation with phytohemagglutinin and with OKT3 antibodies. Studies aimed at characterizing the cellular and molecular basis of the protection afforded to T cells by RBCs showed that (1) optimal protection required intact RBCs and red cell/T-cell contact but not monocytes; (2) RBCs markedly reduced the level of intracellular reactive oxygen species; and (3) RBCs inhibited the formation of protein-bound acrolein, a peroxidation adduct in biologic systems. Overall, these data indicate that human RBCs protect T cells from activation-induced cell death, at least in part by reducing the pro-oxidant state, and suggest a role for RBCs as conceivable modulators of T-cell homeostasis. | lld:pubmed |
| pubmed-article:11342443 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11342443 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342443 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11342443 | pubmed:month | May | lld:pubmed |
| pubmed-article:11342443 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:11342443 | pubmed:author | pubmed-author:UchidaKK | lld:pubmed |
| pubmed-article:11342443 | pubmed:author | pubmed-author:PortoGG | lld:pubmed |
| pubmed-article:11342443 | pubmed:author | pubmed-author:FonsecaA MAM | lld:pubmed |
| pubmed-article:11342443 | pubmed:author | pubmed-author:BROOKB NBN | lld:pubmed |
| pubmed-article:11342443 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11342443 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11342443 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:11342443 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11342443 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11342443 | pubmed:pagination | 3152-60 | lld:pubmed |
| pubmed-article:11342443 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:11342443 | pubmed:meshHeading | pubmed-meshheading:11342443... | lld:pubmed |
| pubmed-article:11342443 | pubmed:meshHeading | pubmed-meshheading:11342443... | lld:pubmed |
| pubmed-article:11342443 | pubmed:meshHeading | pubmed-meshheading:11342443... | lld:pubmed |
| pubmed-article:11342443 | pubmed:meshHeading | pubmed-meshheading:11342443... | lld:pubmed |
| pubmed-article:11342443 | pubmed:meshHeading | pubmed-meshheading:11342443... | lld:pubmed |
| pubmed-article:11342443 | pubmed:meshHeading | pubmed-meshheading:11342443... | lld:pubmed |
| pubmed-article:11342443 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11342443 | pubmed:articleTitle | Red blood cells inhibit activation-induced cell death and oxidative stress in human peripheral blood T lymphocytes. | lld:pubmed |
| pubmed-article:11342443 | pubmed:affiliation | Laboratory of Molecular Immunology, Institute for Molecular and Cell Biology, University of Porto, Portugal. | lld:pubmed |
| pubmed-article:11342443 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11342443 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:11342443 | lld:pubmed |
