pubmed-article:3880774 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3880774 | lifeskim:mentions | umls-concept:C0000768 | lld:lifeskim |
pubmed-article:3880774 | lifeskim:mentions | umls-concept:C0005961 | lld:lifeskim |
pubmed-article:3880774 | lifeskim:mentions | umls-concept:C0596993 | lld:lifeskim |
pubmed-article:3880774 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:3880774 | pubmed:dateCreated | 1985-2-21 | lld:pubmed |
pubmed-article:3880774 | pubmed:abstractText | We studied recovery of peripheral blood- and bone marrow-derived myeloid progenitor cells (CFU-G,M) in 29 patients who received bone marrow transplants 2 mo to 8.5 yr previously. All patients had normal levels of peripheral blood neutrophils, normal bone marrow cellularity, and a normal myeloid-erythroid ratio. Both peripheral blood- and bone marrow-derived CFU-G,M were markedly reduced compared with normal controls and bone marrow donors [5 +/- 1/10(6) vs. 37 +/- 4/10(6) (P less than 0.001) and 23 +/- 5/2 x 10(5) vs. 170 +/- 21/2 x 10(5) (P less than 0.001)]. Five patients had no detectable CFU-G,M even when 10(6) bone marrow cels were plated. These abnormalities of CFU-G,M were unrelated to age, sex, diagnosis, conditioning regimen, dose of bone marrow cells transplanted, and presence or absence of graft-vs.-host disease. Patients who received either autotransplants or transplants from identical twins also had decreased or absent CFU-G,M indicating that allogeneic factors and posttransplant immune suppressor with methotrexate or corticosteroids were not major determinants of this abnormality. Co-culture of normal or donor peripheral blood or bone marrow mononuclear cells with recipients peripheral blood or bone marrow mononuclear cells, purified T cells, or serum failed to show any evidence of active CFU-G,M suppression. Furthermore, the abnormality of CFU-G,M could not be corrected by the addition of normal syngeneic (donor) hematopoietic cells or serum. Depletion of T-cells from recipient bone marrow by physical techniques resulted in marked increase in CFU-G,M (36 +/- 13 vs. 138 +/- 36; P less than 0.05). The abnormality could be reproduced in vitro by readdition of autologous T cells. In contrast to results with T cell depletion by physical techniques, T cell depletion with a monoclonal anti-T antibody (B7) and complement had no effect. These data indicate that most-transplant recipients have a marked abnormality in CFU-G,M when these cells are cultured in vitro. In at least some of these patients, the decreased cloning efficiency of CFU-G,M appears to be mediated by a suppressive effect of autologous T cells. | lld:pubmed |
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pubmed-article:3880774 | pubmed:language | eng | lld:pubmed |
pubmed-article:3880774 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3880774 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:3880774 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3880774 | pubmed:month | Jan | lld:pubmed |
pubmed-article:3880774 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:3880774 | pubmed:author | pubmed-author:LUGG | lld:pubmed |
pubmed-article:3880774 | pubmed:author | pubmed-author:GaleR PRP | lld:pubmed |
pubmed-article:3880774 | pubmed:author | pubmed-author:FitchenJ HJH | lld:pubmed |
pubmed-article:3880774 | pubmed:author | pubmed-author:ChamplinRR | lld:pubmed |
pubmed-article:3880774 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3880774 | pubmed:volume | 75 | lld:pubmed |
pubmed-article:3880774 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3880774 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3880774 | pubmed:pagination | 234-41 | lld:pubmed |
pubmed-article:3880774 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:3880774 | pubmed:year | 1985 | lld:pubmed |
pubmed-article:3880774 | pubmed:articleTitle | Abnormalities of myeloid progenitor cells after "successful" bone marrow transplantation. | lld:pubmed |
pubmed-article:3880774 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:3880774 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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