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Coregulation of the APO-1 antigen with intercellular adhesion molecule- 1
(CD54) in tonsillar B cells and coordinate expression in follicular center
B cells and in follicle center and mediastinal B-cell lymphomas
P Moller, C Henne, F Leithauser, A Eichelmann, A Schmidt, S Bruderlein, J Dhein and PH Krammer
Institute of Pathology, University of Heidelberg, Germany.
APO-1 is a 48-Kd transmembrane glycoprotein identical to the Fas antigen
and belongs to the nerve growth factor (NGF)/tumor necrosis factor (TNF)
receptor family of surface molecules. Cross-linking of APO- 1 induces
apoptotic cell death in sensitive cells. We show here that APO-1 is an
activation molecule on B cells. It was induced/enhanced on dense and
buoyant tonsillar B cells, respectively, through surface Ig cross-linking
in combination with interleukin-2 or by interferon-gamma together with
tumor necrosis factor-alpha. These conditions also increased the amount of
intercellular adhesion molecule-1 (CD54) on these cells. Epstein-Barr virus
transformants of peripheral B cells coexpressed APO-1 and CD54 at very high
levels. Immunohistologically, Apo-1 was detectable at low levels in a
subpopulation of follicle center B blasts and, at higher levels, in
sinusoidal B cells. APO-1 was undetectable in follicular mantle B cells and
plasma cells. In isolated tonsillar B cells, APO-1 was expressed in CD10+
follicle center cells. In acute B lymphoblastic leukemia, chronic B
lymphocytic leukemia, and Burkitt's lymphomas, APO-1 and CD54 molecules
were immunohistochemically undetectable. Coordinate expression of these
antigens was found in mediastinal B-cell lymphomas. The mode of APO-1 and
CD54 expression was correlated in follicle center cell lymphomas (P <
.0019), but less stringently in hairy cell leukemia. No association was
found in plasmacytomas. This was in line with the differential expression
of these molecules found in reactive plasma cells. Expression of APO-1 in B
cells of different stages of differentiation and, correspondingly, in
certain B-cell neoplasias might suggest a role of this molecule in the
induction of B-cell apoptosis. This function might be influenced by CD54
and CD54-mediated signals.
Volume 81,
Issue 8,
pp. 2067-2075,
04/15/1993
Copyright © 1993 by The American Society of Hematology

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