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
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
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.