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Cutting Edge |
-Induced Suppression of B Lymphocyte Formation1




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* First Department of Internal Medicine, Faculty of Medicine,
Medicine and Biosystemic Science and
Anatomical Pathology, Graduate School of Medical Sciences,
Department of Medical Technology, School of Health Sciences, and
¶ Department of Molecular and Cellular Biology, Laboratory of Embryonic and Genetic Engineering, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan;
|| Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan;
# Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan; and
** Core Research for Engineering, Science, and Technology, Japan Science and Technology Corporation, Saitama, Japan
IFN-
inhibits B lymphocyte development, and the nuclear
protein Daxx has been reported to be essential for this biological
activity. We show in this study that IFN-
inhibits the clonal
proliferation of B lymphocyte progenitors in response to IL-7 in
wild-type, but not in tyk2-deficient, mice. In addition,
the IFN-
-induced up-regulation and nuclear translocation of
Daxx are completely abrogated in the absence of tyk2. Therefore,
tyk2 is directly involved in IFN-
signaling for the induction and
translocation of Daxx, which may result in B lymphocyte growth arrest
and/or apoptosis.
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