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Blood, Vol. 93 No. 2 (January 15), 1999:
pp. 617-623
Tumor Necrosis Factor Receptor-Associated Factor 1 Is Overexpressed
in Reed-Sternberg Cells of Hodgkin's Disease and
Epstein-Barr Virus-Transformed Lymphoid Cells
Horst Dürkop,
Hans-Dieter Foss,
Gudrun Demel,
Heike Klotzbach,
Corinna Hahn, and
Harald Stein
From the Institut für Pathologie, UK Benjamin Franklin, Freie
Universität Berlin, Berlin, Germany.
The tumor necrosis factor (TNF) receptor-associated factor 1 (TRAF1)
is a member of the recently defined TRAF family. It takes part in the
signal transduction of the TNF receptor 2 (TNFR2), the lymphotoxin-
receptor (LT-R), CD40, CD30, and LMP1; is induced by LMP1 in vitro;
and protects lymphoid cells from apoptosis. To identify the cells in
which TRAF1 is active in vivo, we studied TRAF1 transcripts in normal
lymphoid tissue, in Epstein-Barr virus (EBV)-induced
lymphoproliferations, and in malignant lymphomas with special reference
to those that overexpress the cytokine receptor CD30 and CD40 of the
TNF receptor family at the single-cell level using a radioactive in
situ hybridization. In normal lymphoid tissue, TRAF1 message proved to
be absent from all resting B and T cells as well as from macrophages
and accessory cells (follicular dendritic cells and interdigitating
cells) and present in few perifollicular and intrafollicular lymphoid
blasts. In contrast, there was a high and consistent TRAF1
overexpression in EBV-induced lymphoproliferations and Hodgkin's
disease. Nearly all non-Hodgkin's lymphoma show low or no TRAF1
expression. Only some cases of diffuse large B-cell lymphoma showed a
moderate to high TRAF1 signal. Several of the latter cases were
EBV+. These data confirm that TRAF1 is an inducible
molecule and indicates its deregulation in the mentioned disorders with
the potential of a blockage of the apoptotic pathway.
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