演題詳細

ポスター / Poster

【E】ポスター 43 (Poster 43) :GVHD/Chimerism

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日程
2013年10月11日(金)
時間
16:50 - 17:50
会場
ポスター会場 / Poster (ロイトン札幌 3F エメラルドABCD)
座長・司会
岡本 康裕 (Yasuhiro Okamoto):1
1:Department of Pediatrics, Kagoshima University Hospital, Japan
 
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Indoleamine 2,3-dioxygenase plays a critical role in prevention of idiopathic pneumonia syndrome

演題番号 : PS-1-325

Su-Kil Seo:1、Soung-Min Lee:1、Won Sik Lee:2、Young Don Joo:3

1:Department of Microbiology and Immunology, College of Medicine, Inje University, Republic of Korea、2:Department of Hemato/Oncology, Busan Paik Hospital, College of Medicine, Inje University, Republic of Korea、3:Department of Hemato/Oncology, Haeundae Paik Hospital, College of Medicine, Inje University, Republic of Korea

 

Graft-versus-host disease (GVHD) is mediated by donor T cells which preferentially damaged in the skin, gastrointestinal (GI) tract, liver, and lung. Idiopathic pneumonia syndrome (IPS) is an acute noninfectious lung injury that is associated with absence of IFN-γ. However, the protective mechanisms of IFN-γ on IPS are still largely unknown. In this study, we demonstrated that indoleamine 2,3-dioxygenase (IDO), tryptophan depleting enzyme, is a critical for protecting IPS by IFN-γ. We initially found that IDO was strongly induced in epithelial cells from both colon and lung tissue of recipient mice by IFN-γ generated from donor T cells at 7-14 days after transplantation. Severity and mortality in acute GVHD were higher in IDO-/- recipient mice compared with wild-type. Unexpectedly, that was mainly caused by lung injury rather than colon damage. Although IFN-γ levels were similar, IL-4 and TNF-γ levels in lung tissue of IDO-/- recipient mice were marked increased. Recipient mice transplanted with donor graft of IFN-γ-/- have severe symptoms of IPS and no IDO expression. After administration with recombinant IFN-γ at 5 and 7 days after transplantation, IDO was induced in lung tissue, which led decreasing tissue damage and IL-4 levels. These results demonstrate that IFN-γ-induced IDO expression in lung epithelial cells is critical for the prevention of IPS, suggesting IDO be adequate as a potential therapeutic target for prevention and treatment of IPS.

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