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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Synthetic tryptophan metabolite 3,4-DAA reduces acute GVHD through modulation of DC function

演題番号 : PS-1-326

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

1:Department of Hematology, Busan Paik Hospital, Inje University, Busan, Korea、2:Department of Hematology, Haeundae Paik Hospital, Inje University, Busan, Korea、3:Department of Microbiology and Immunology, Inje University, Busan, Korea

 

Accumulation of “danger signals” by chemo- or radio-chemotherapy leads to activate host antigen presenting cells (APCs) which play a central role of allogeneic T cell priming. Therefore, targeting APC or APC function is an attractive strategy to regulate the course of GVHD. Anti-allergic drug N-(3,4,-Dimethoxycinnamoyl) anthranilic acid (3,4-DAA), synthetic derivative of the tryptophan metabolite anthranilic acid, has been reported its immunomodulatory activities of APC function on several autoimmune mouse models. However, its effects have not been yet reported in GVHD. To determine the efficacy of 3,4-DAA on regulating host APCs, we administrated 3,4-DAA into allogeneic recipient mice prior to total body irradiation and BMT. There was significantly improved survival of recipient mice from lethal acute GVHD. We found that 3,4-DAA treatment significantly reduced IL-12, IL-6, and TNF-alpha production in bone marrow-derived DCs (BMDCs) stimulated with LPS. Maturation markers involved in CD40, CD80, CD86, and I-A also significantly reduced. Moreover, 3, 4-DAA decreased the ability of DCs to stimulate allogeneic T cell activation and differentiation by in vitro and in vivo treatment. Our results suggest 3,4-DAA and their derivatives offer a new strategy for preventing acute GVHD.

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