| Autor: |
Karadimitris A; Department of Human Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA., Li K, Notaro R, Araten DJ, Nafa K, Thertulien R, Ladanyi M, Stevens AE, Rosenfeld CS, Roberts IA, Luzzatto L |
| Jazyk: |
angličtina |
| Zdroj: |
British journal of haematology [Br J Haematol] 2001 Dec; Vol. 115 (4), pp. 1010-4. |
| DOI: |
10.1046/j.1365-2141.2001.03172.x |
| Abstrakt: |
There is mounting evidence to suggest that T-cell-mediated suppression of haemopoiesis is a pathogenetic mechanism in three bone marrow failure syndromes: aplastic anaemia (AA), paroxysmal nocturnal haemoglobinuria (PNH) and myelodysplasia (MDS). T-cell microclones can be detected by sensitive polymerase chain reaction (PCR)-based methods in all three disorders. Recently, larger clonal populations of T-cell large granular lymphocytes (T-LGLs) have been observed in some patients with AA and MDS. Here, we report the development of a large clonal T-LGL population in a patient with bona fide PNH. In this patient, we defined part of the sequence of the T-cell receptor (TCR) beta-chain gene, and we have shown that the large T-LGL population emerged from a background of multiple smaller T-cell clones. Thus, T-LGL clones in AA, MDS and PNH probably expand as a result of antigenic stimulation. It is postulated that the antigen driving clonal T-cell proliferations in these disorders exists on haemopoietic stem cells. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
Plný text