FullText URL blood_119_1_285.pdf
Author 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|
Abstract 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.
Note This research was originally published in Blood. 2012. © the American Society of Hematology.
Published Date 2012-01-05
Publication Title Blood
Volume volume119
Issue issue1
Start Page 285
End Page 295
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
File Version publisher
PubMed ID 22077062
DOI 10.1182/blood-2011-01-332478
Web of Sience KeyUT 000299012400035
Related Url https://doi.org/10.1182/blood-2011-01-332478