Analysis of T-cell subpopulations in T-cell non-Hodgkin's lymphoma of angioimmunoblastic lymphadenopathy with dysproteinemia type by single target gene amplification of T cell receptor-beta gene rearrangements

Citation
K. Willenbrock et al., Analysis of T-cell subpopulations in T-cell non-Hodgkin's lymphoma of angioimmunoblastic lymphadenopathy with dysproteinemia type by single target gene amplification of T cell receptor-beta gene rearrangements, AM J PATH, 158(5), 2001, pp. 1851-1857
Citations number
39
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
AMERICAN JOURNAL OF PATHOLOGY
ISSN journal
00029440 → ACNP
Volume
158
Issue
5
Year of publication
2001
Pages
1851 - 1857
Database
ISI
SICI code
0002-9440(200105)158:5<1851:AOTSIT>2.0.ZU;2-P
Abstract
Angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) is defined in the current lymphoma classifications as a T-cell non-Hodgkin's lymphoma. H owever, in approximately one third of the cases of this lymphoproliferative disease rearrangements of T-cell receptor (TCR) genes indicating clonal ex pansion of T cells are not detectable, It is currently believed that these cases may represent early stages of a lymphoma with a minor oligoclonal T-c ell population. In the present study, 18 lymph nodes with the characteristi c histology of AILD were investigated for clonal T-cell receptor gene rearr angements by analysis of DNA extracted from whole tissue sections. Dominant T-cell clones mere detected in 12 of these cases. Single CD4(+) and CDS' T cells and proliferating Ki67(+) cells of seven cases were micromanipulated from frozen tissue sections. TCR beta gene rearrangements mere amplified f rom these cells by polymerase chain reaction and sequenced. In all informat ive cases, the clonal gene rearrangements mere only detected among CD4(+), and not among CD8(+) T cells, indicating that the tumor clones in AILD usua lly derive from CD4(+) T cells, Minor clonal T-cell populations in those ca ses in which no clone was found by whole-tissue DNA analysis mere not detec table even at single cell resolution. T-cell clones in 4 of 10 cases were f ound to express similar TCR beta chains, indicating a potential role of (su per) antigen triggering in at least some cases of AILD.