-
- Tiejun Zhao
- Laboratory of Virus Control, Institute for Virus Research, Kyoto University, Kyoto, Japan;
-
- Yorifumi Satou
- Laboratory of Virus Control, Institute for Virus Research, Kyoto University, Kyoto, Japan;
-
- Kenji Sugata
- Laboratory of Virus Control, Institute for Virus Research, Kyoto University, Kyoto, Japan;
-
- Paola Miyazato
- Laboratory of Virus Control, Institute for Virus Research, Kyoto University, Kyoto, Japan;
-
- Patrick L. Green
- Center for Retrovirus Research and Departments of Veterinary Biosciences and Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, OH;
-
- Takeshi Imamura
- Department of Molecular Medicine for Pathogenesis, Ehime University Graduate School of Medicine, Ehime, Japan;
-
- Masao Matsuoka
- Laboratory of Virus Control, Institute for Virus Research, Kyoto University, Kyoto, Japan;
抄録
<jats:title>Abstract</jats:title><jats:p>Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus that is etiologically associated with adult T-cell leukemia. The HTLV-1 bZIP factor (HBZ), which is encoded by the minus strand of the provirus, is involved in both regulation of viral gene transcription and T-cell proliferation. We showed in this report that HBZ interacted with Smad2/3, and enhanced transforming growth factor-β (TGF-β)/Smad transcriptional responses in a p300-dependent manner. The N-terminal LXXLL motif of HBZ was responsible for HBZ-mediated TGF-β signaling activation. In a serial immunoprecipitation assay, HBZ, Smad3, and p300 formed a ternary complex, and the association between Smad3 and p300 was markedly enhanced in the presence of HBZ. In addition, HBZ could overcome the repression of the TGF-β response by Tax. Finally, HBZ expression resulted in enhanced transcription of Pdgfb, Sox4, Ctgf, Foxp3, Runx1, and Tsc22d1 genes and suppression of the Id2 gene; such effects were similar to those by TGF-β. In particular, HBZ induced Foxp3 expression in naive T cells through Smad3-dependent TGF-β signaling. Our results suggest that HBZ, by enhancing TGF-β signaling and Foxp3 expression, enables HTLV-1 to convert infected T cells into regulatory T cells, which is thought to be a critical strategy for virus persistence.</jats:p>
収録刊行物
-
- Blood
-
Blood 118 (7), 1865-1876, 2011-08-18
American Society of Hematology
- Tweet
詳細情報 詳細情報について
-
- CRID
- 1360002218954763776
-
- NII論文ID
- 20001178490
- 10030768333
-
- ISSN
- 15280020
- 00064971
-
- データソース種別
-
- Crossref
- CiNii Articles
- KAKEN