Author
Listed:
- Takashi Satoh
(Laboratory of Host Defense, WPI Immunology Frontier Research Center (WPI IFReC), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan
Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Hiroyasu Kidoya
(Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Hisamichi Naito
(Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Masahiro Yamamoto
(Laboratory of immunoparasitology, WPI Immunology Frontier Research Center (WPI IFReC), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan
Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Naoki Takemura
(Laboratory of Host Defense, WPI Immunology Frontier Research Center (WPI IFReC), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan
Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Katsuhiro Nakagawa
(Laboratory of Host Defense, WPI Immunology Frontier Research Center (WPI IFReC), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan
Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Yoshichika Yoshioka
(Laboratory of Biofunctional Imaging, WPI Immunology Frontier Research Center (WPI IFReC), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Eiichi Morii
(Graduate School of Medicine, Osaka University, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Nobuyuki Takakura
(Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Osamu Takeuchi
(Laboratory of Host Defense, WPI Immunology Frontier Research Center (WPI IFReC), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan
Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan
Laboratory of Infection and Prevention, Institute for Virus Research, Kyoto University, 53 Shogoin Kawara-cho, Sakyo-ku, Kyoto 606-8507, Japan)
- Shizuo Akira
(Laboratory of Host Defense, WPI Immunology Frontier Research Center (WPI IFReC), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan
Research Institute for Microbial Diseases (RIMD), Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan)
Abstract
Haematopoietic expression of the adaptor protein Trib1 is shown to be required for the presence of adipose-tissue-resident macrophages with an M2-like phenotype; Trib1 deficiency leads to aberrant expression of C/EBPα and impaired adipose tissue function.
Suggested Citation
Takashi Satoh & Hiroyasu Kidoya & Hisamichi Naito & Masahiro Yamamoto & Naoki Takemura & Katsuhiro Nakagawa & Yoshichika Yoshioka & Eiichi Morii & Nobuyuki Takakura & Osamu Takeuchi & Shizuo Akira, 2013.
"Critical role of Trib1 in differentiation of tissue-resident M2-like macrophages,"
Nature, Nature, vol. 495(7442), pages 524-528, March.
Handle:
RePEc:nat:nature:v:495:y:2013:i:7442:d:10.1038_nature11930
DOI: 10.1038/nature11930
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