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*
Department of Pathology and Kaplan Comprehensive Cancer Center, New York University Medical Center, New York, NY 10016;
Department of Anatomic Pathology, University of Torino, Torino, Italy; Divisions of
Pediatric Hematology/Oncology and
§
Hematology/Oncology, Department of Medicine, New York University Medical Center, New York, NY 10016; and
¶
Department of Microbiology, Miami University, Miami, FL 33101
The biological function of CD30 in the thymus has been only
partially elucidated, although recent data indicate that it may be
involved in negative selection. Because CD30 is expressed only by a
small subpopulation of medullary thymocytes, we generated transgenic
(Tg) mice overexpressing CD30 in T lymphocytes to further address its
role in T cell development. CD30 Tg mice have normal thymic size with a
normal number and subset distribution of thymocytes. In vitro, in the
absence of CD30 ligation, thymocytes of CD30 Tg mice have normal
survival and responses to apoptotic stimuli such as radiation,
dexamethasone, and Fas. However, in contrast to controls, CD30 Tg
thymocytes are induced to undergo programmed cell death (PCD) upon
cross-linking of CD30, and the simultaneous engagement of TCR and CD30
results in a synergistic increase in thymic PCD. CD30-mediated PCD
requires caspase 1 and caspase 3, is not associated with the activation
of NF-
B or c-Jun, but is totally prevented by Bcl-2. Furthermore,
CD30 overexpression enhances the deletion of
CD4+/CD8+ thymocytes induced by staphylococcal
enterotoxin B superantigen and specific peptide. These findings suggest
that CD30 may act as a costimulatory molecule in thymic negative
selection.
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