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Short Communications |
From the Department of Pathology,*
Division of
Hematopathology, Vanderbilt University Medical Center, Nashville,
Tennessee, and the Department of Pathology and Laboratory
Medicine,
Allegheny University of the Health
Sciences, MCP-Hahnemann School of Medicine, Philadelphia, Pennsylvania
The factor(s) responsible for the reduced B cell number and
increased T cell infiltrate in T-cell-rich large-B-cell lymphomas
(TCRBCLs) have not been well characterized. We studied 18 TCRBCLs and
12 diffuse large-B-cell lymphomas (DLBCLs) to compare the 1)
predominant T cell subpopulation(s), 2) expression of cytotoxic
granule proteins (TIA-1 and granzyme B), 3) level of tumor cell
apoptosis (Apoptag system, Oncor, Gaithersburg,
MD), and 4) expression of Ki-67 (Mib-1) and apoptosis-related
proteins (fas (CD95), bcl-2, and p53). T cells in
TCRBCLs and DLBCLs were predominantly CD8+ T cells
expressing
ß T-cell receptors and TIA-1 (16 of 18 TCRBCLs with
>50% TIA-1+ small lymphocytes) but lacking granzyme B (16
of 18 TCRBCLs with <25% granzyme B+ small lymphocytes).
Scattered apoptotic tumor cells (confirmed with CD20 co-labeling) were
present in 15 of 18 TCRBCLs, with 14 of 15 cases having <10%
apoptotic cells. No apoptotic cells were seen in 12 of 12 DLBCLs. In 16
of 16 immunoreactive TCRBCLs, <25% tumor cells were
bcl-2+, whereas 6 of 12 DLBCLs had >50%
bcl-2+ tumor cells. CD95 (fas) expression was also
lower, with 3 of 18 (16.7%) TCRBCLs versus 4 of
12 (33%) DLBCLs having >25% CD95+ tumor cells. TCRBCLs
and DLBCLs had similar levels of p53 and Ki-67 (Mib-1) expression.
Thus, T cells in TCRBCLs are non-activated cytotoxic T
lymphocytes (TIA-1+, granzyme B-).
Tumor cell apoptosis (perhaps cytotoxic T cell mediated) may partly
account for the decreased number of large (neoplastic) B cells in
TCRBCLs, but other factors (ie, decreased bcl-2
expression) may also be needed.
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