| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Regular Articles |



From the Senckenberg Institute of Pathology,*
University
of Frankfurt, Frankfurt am Main; the Department of Dermatology and
Venerology
and the Institute for
Genetics and Department of Internal Medicine I,¶
University of Cologne, Cologne; the Institute of Transfusion Medicine
and Immunohaematology,
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-Hodgkins 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.
This article has been cited by other articles:
![]() |
E. Geissinger, I. Bonzheim, L. Krenacs, S. Roth, P. Strobel, G. Ott, P. Reimer, M. Wilhelm, H. K. Muller-Hermelink, and T. Rudiger Identification of the Tumor Cells in Peripheral T-Cell Lymphomas by Combined Polymerase Chain Reaction-Based T-Cell Receptor {beta} Spectrotyping and Immunohistological Detection with T-Cell Receptor {beta} Chain Variable Region Segment-Specific Antibodies J. Mol. Diagn., October 1, 2005; 7(4): 455 - 464. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. R. Brown and A. T. Skarin Clinical Mimics of Lymphoma Oncologist, July 1, 2004; 9(4): 406 - 416. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Weidmann, M. Gramatzki, M. Wilhelm, and P. S. Mitrou Diagnosis and actual therapy strategies in peripheral T-cell lymphomas: summary of an international meeting Ann. Onc., March 1, 2004; 15(3): 369 - 374. [Full Text] [PDF] |
||||
![]() |
L. Krenacs, M. J. Smyth, E. Bagdi, T. Krenacs, L. Kopper, T. Rudiger, A. Zettl, H. K. Muller-Hermelink, E. S. Jaffe, and M. Raffeld The serine protease granzyme M is preferentially expressed in NK-cell, gamma delta T-cell, and intestinal T-cell lymphomas: evidence of origin from lymphocytes involved in innate immunity Blood, May 1, 2003; 101(9): 3590 - 3593. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |