フルテキストURL blood_119_1_285.pdf
著者 Nishimori, Hisakazu| Maeda, Yoshinobu| Teshima, Takanori| Sugiyama, Haruko| Kobayashi, Koichiro| Yamasuji, Yoshiko| Kadohisa, Sachiyo| Uryu, Hidetaka| Takeuchi, Kengo| Tanaka, Takehiro| Yoshino, Tadashi| Iwakura, Yoichiro| Tanimoto, Mitsune|
抄録 Chronic GVHD (cGVHD) is a main cause of late death and morbidity after allogeneic hematopoietic cell transplantation, but its pathogenesis remains unclear. We investigated the roles of Th subsets in cGVHD with the use of a well-defined mouse model of cGVHD. In this model, development of cGVHD was associated with up-regulated Th1, Th2, and Th17 responses. Th1 and Th2 responses were up-regulated early after BM transplantation, followed by a subsequent up-regulation of Th17 cells. Significantly greater numbers of Th17 cells were infiltrated in the lung and liver from allogeneic recipients than those from syngeneic recipients. We then evaluated the roles of Th1 and Th17 in cGVHD with the use of IFN-γ-deficient and IL-17-deficient mice as donors. Infusion of IFN-γ(-/-) or IL-17(-/-) T cells attenuated cGVHD in the skin and salivary glands. Am80, a potent synthetic retinoid, regulated both Th1 and Th17 responses as well as TGF-β expression in the skin, resulting in an attenuation of cutaneous cGVHD. These results suggest that Th1 and Th17 contribute to the development of cGVHD and that targeting Th1 and Th17 may therefore represent a promising therapeutic strategy for preventing and treating cGVHD.
備考 This research was originally published in Blood. 2012. © the American Society of Hematology.
発行日 2012-01-05
出版物タイトル Blood
119巻
1号
開始ページ 285
終了ページ 295
資料タイプ 学術雑誌論文
言語 English
OAI-PMH Set 岡山大学
著作権者 https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
論文のバージョン publisher
PubMed ID 22077062
DOI 10.1182/blood-2011-01-332478
Web of Sience KeyUT 000299012400035
関連URL https://doi.org/10.1182/blood-2011-01-332478