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Myeloid differentiation factor 88 signaling in donor T cells accelerates graft-versus-host disease

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Title: Myeloid differentiation factor 88 signaling in donor T cells accelerates graft-versus-host disease
Authors: Matsuoka, Satomi Browse this author
Hashimoto, Daigo Browse this author →KAKEN DB
Kadowaki, Masanori Browse this author
Ohigashi, Hiroyuki Browse this author
Hayase, Eiko Browse this author
Yokoyama, Emi Browse this author
Hasegawa, Yuta Browse this author
Tateno, Takahiro Browse this author
Chen, Xuanzhong Browse this author
Aoyama, Kazutoshi Browse this author
Oka, Hideyo Browse this author
Onozawa, Masahiro Browse this author →KAKEN DB
Takeda, Kiyoshi Browse this author →KAKEN DB
Akashi, Koichi Browse this author →KAKEN DB
Teshima, Takanori Browse this author →KAKEN DB
Issue Date: 1-Jan-2020
Publisher: Ferrata Storti Foundation
Journal Title: Haematologica
Volume: 105
Issue: 1
Start Page: 226
End Page: 234
Publisher DOI: 10.3324/haematol.2018.203380
Abstract: Myeloid differentiation factor 88 (MyD88) signaling has a crucial role in activation of both innate and adoptive immunity. MyD88 transduces signals via Toll-like receptor and interleukin-1 receptor superfamily to the NF kappa B pathway and inflammasome by forming a molecular complex with interleukin-1 receptor-associated kinase 4. The MyD88/interleukin-1 receptor-associated kinase 4 pathway plays an important role, not only in innate immunity, but also T-cell immunity; however, its role in donor T cells on the pathophysiology of graft-versus-host disease (GvHD) remains to be elucidated. We addressed this issue by using MyD88-deficient T cells in a mouse model of allogeneic hematopoietic stem cell transplantation (allo-SCT). While MyD88-deficient and wild-type T cells proliferated equivalently after transplantation, MyD88-deficient T cells demonstrated impaired survival and differentiation toward Th1, Tc1, and Th17, and induced less severe GvHD compared to wild-type T cells. Administration of interleukin-1 receptor-associated kinase 4 inhibitor PF-06650833 significantly ameliorated GvHD after allo-SCT. These results thus demonstrate that donor T-cell receptor-associated kinase 4 pathway is a novel therapeutic target against GvHD after allo-SCT.
Rights: https://creativecommons.org/licenses/by-nc/4.0/
Type: article
URI: http://hdl.handle.net/2115/76613
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

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