Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions |
umls-concept:C0003442,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0026986,
umls-concept:C0030705,
umls-concept:C0034790,
umls-concept:C0314589,
umls-concept:C0332281,
umls-concept:C0871261,
umls-concept:C1515926,
umls-concept:C1517945,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1979963,
umls-concept:C2003903,
umls-concept:C2911692
|
pubmed:issue |
5
|
pubmed:dateCreated |
1998-11-17
|
pubmed:abstractText |
We have demonstrated that 44% of myelodysplastic syndrome (MDS) patients with cytopenia have a haematological response to antithymocyte globulin (ATG). Three ATG responders and two non-responders with refractory anaemia were further studied for lymphocyte-mediated inhibition of bone marrow using a standard CFU-GM assay. In responders, peripheral blood lymphocytes (PBL) added at a 5:1 ratio suppressed CFU-GM by 54+/-9% (P=0.04) and was reversed by ATG treatment. Pre-treatment marrow depleted of CD3 lymphocytes, increased CFU-GM by 32% (P=0.02) in an ATG responder, but not in a non-responder. CD3 lymphocytes from 6-month post-treatment marrow did not inhibit pre-treatment CFU-GM, indicating ATG had affected the T cells. Pre-treatment marrow depleted of CD8 lymphocytes, increased CFU-GM by 60% (P=0.01) and 49% (P=0.03) in two ATG responders, but not in a non-responder. Inhibition required cell-cell interaction through MHCI. TCRVbeta families, analysed by SSCP, changed from clonal to polyclonal in one ATG responder after 6 months, but clones persisted in a non-responder. These results indicate patients with refractory anaemia who respond to ATG have CD8 T-cell clones that mediate MHCI-restricted suppression of CFU-GM which are replaced by polyclonal T cells that do not suppress CFU-GM after ATG treatment.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
0007-1048
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
102
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1314-22
|
pubmed:dateRevised |
2004-11-17
|
pubmed:meshHeading |
pubmed-meshheading:9753062-Adult,
pubmed-meshheading:9753062-Antilymphocyte Serum,
pubmed-meshheading:9753062-Bone Marrow Cells,
pubmed-meshheading:9753062-CD8-Positive T-Lymphocytes,
pubmed-meshheading:9753062-Colony-Forming Units Assay,
pubmed-meshheading:9753062-Female,
pubmed-meshheading:9753062-Humans,
pubmed-meshheading:9753062-Lymphopenia,
pubmed-meshheading:9753062-Male,
pubmed-meshheading:9753062-Middle Aged,
pubmed-meshheading:9753062-Myelodysplastic Syndromes,
pubmed-meshheading:9753062-Receptors, Antigen, T-Cell,
pubmed-meshheading:9753062-T-Lymphocyte Subsets,
pubmed-meshheading:9753062-T-Lymphocytes
|
pubmed:year |
1998
|
pubmed:articleTitle |
Haematological response of patients with myelodysplastic syndrome to antithymocyte globulin is associated with a loss of lymphocyte-mediated inhibition of CFU-GM and alterations in T-cell receptor Vbeta profiles.
|
pubmed:affiliation |
Department of Blood and Marrow Transplantation, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.
|
pubmed:publicationType |
Journal Article
|