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(American Journal of Pathology. 2001;158:1851-1857.)
© 2001 American Society for Investigative Pathology


Regular Articles

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- ß Gene Rearrangements

Klaus Willenbrock*, Axel Roers{dagger}, Christian Seidl{ddagger}, Hans-Heinrich Wacker§, Ralf Küppers and Martin-Leo Hansmann*

From the Senckenberg Institute of Pathology,*
University of Frankfurt, Frankfurt am Main; the Department of Dermatology and Venerology{dagger}
and the Institute for Genetics and Department of Internal Medicine I,
University of Cologne, Cologne; the Institute of Transfusion Medicine and Immunohaematology,{ddagger}
Red Cross Blood Donor Service Hessen, Frankfurt/Main; and the Institute of Pathology,§
University of Kiel, Kiel, Germany

Angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) is defined in the current lymphoma classifications as a T-cell non-Hodgkin’s lymphoma. However, in approximately one third of the cases of this lymphoproliferative disease rearrangements of T-cell receptor (TCR) genes indicating clonal expansion 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-cell population. In the present study, 18 lymph nodes with the characteristic histology of AILD were investigated for clonal T-cell receptor gene rearrangements by analysis of DNA extracted from whole tissue sections. Dominant T-cell clones were detected in 12 of these cases. Single CD4+ and CD8+ T cells and proliferating Ki67+ cells of seven cases were micromanipulated from frozen tissue sections. TCRß gene rearrangements were amplified from these cells by polymerase chain reaction and sequenced. In all informative cases, the clonal gene rearrangements were only detected among CD4+, and not among CD8+ T cells, indicating that the tumor clones in AILD usually derive from CD4+ T cells. Minor clonal T-cell populations in those cases in which no clone was found by whole-tissue DNA analysis were not detectable even at single cell resolution. T-cell clones in 4 of 10 cases were found to express similar TCRß chains, indicating a potential role of (super) antigen triggering in at least some cases of AILD.





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