TY - JOUR
T1 - Cutting edge
T2 - Tyk2 is required for the induction and nuclear translocation of Daxx which regulates IFN-α-induced suppression of B lymphocyte formation
AU - Shimoda, Kazuya
AU - Kamesaki, Kenjirou
AU - Numata, Akihiko
AU - Aoki, Kenichi
AU - Matsuda, Tadashi
AU - Oritani, Kenji
AU - Tamiya, Sadafumi
AU - Kato, Kouji
AU - Takase, Ken
AU - Imamura, Rie
AU - Yamamoto, Tetsuya
AU - Miyamoto, Toshihiro
AU - Nagafuji, Koji
AU - Gondo, Hisashi
AU - Nagafuchi, Seiho
AU - Nakayama, Kei Ichi
AU - Harada, Mine
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2002/11/1
Y1 - 2002/11/1
N2 - IFN-α 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-α 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-α-induced up-regulation and nuclear translocation of Daxx are completely abrogated in the absence of tyk2. Therefore, tyk2 is directly involved in IFN-α signaling for the induction and translocation of Daxx, which may result in B lymphocyte growth arrest and/or apoptosis.
AB - IFN-α 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-α 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-α-induced up-regulation and nuclear translocation of Daxx are completely abrogated in the absence of tyk2. Therefore, tyk2 is directly involved in IFN-α signaling for the induction and translocation of Daxx, which may result in B lymphocyte growth arrest and/or apoptosis.
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U2 - 10.4049/jimmunol.169.9.4707
DO - 10.4049/jimmunol.169.9.4707
M3 - Article
C2 - 12391177
AN - SCOPUS:0036838538
SN - 0022-1767
VL - 169
SP - 4707
EP - 4711
JO - Journal of Immunology
JF - Journal of Immunology
IS - 9
ER -