オクニシ　カツヒデ   Okunishi Katsuhide   奥西　勝秀    所属   東邦大学  医学部 医学科    職種   教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Splenic dendritic cells induced by oral antigen administration are important for the transfer of oral tolerance in an experimental model of asthma.
掲載誌名	正式名：Journal of immunology (Baltimore, Md. : 1950) ISSNコード：0022-1767/1550-6606
掲載区分	国外
出版社	AMER ASSOC IMMUNOLOGISTS
巻・号・頁	176(3),pp.1481-9
著者・共著者	Katsuya Nagatani,Makoto Dohi,Yasuo To,Ryoichi Tanaka,Katsuhide Okunishi,Kazuyuki Nakagome,Kayo Sagawa,Yudo Tanno,Yoshinori Komagata,Kazuhiko Yamamoto
発行年月	2006/02/01
概要	Peripheral tolerance can be induced after the feeding of Ag, which is referred to as oral tolerance. We demonstrated in this study that the oral administration of OVA induced tolerance in an experimental model of asthma in mice, and investigated which cells function as the regulatory cells in the transfer of this oral tolerance. In OVA-fed mice, the percentage of eosinophils in bronchoalveolar lavage fluid, serum IgE levels, airway hyperresponsiveness, and mRNA levels of IL-13 and eotaxin were significantly lower than found in nonfed mice. Histological examination of lung tissue showed a suppression of the accumulation of inflammatory cells in the peribronchial area of OVA-fed mice. Feeding after the first immunization or between the first and the second immunization suppressed these findings, whereas feeding just before the airway Ag challenge did not. The suppression of disease in OVA-fed mice was successfully transferred by injection of whole spleen cells of OVA-fed mice. When CD11c+ dendritic cells (DCs) were removed from splenocytes, this transfer of suppression was completely abolished. The injection of splenic DCs purified from OVA-fed mice alone transferred the suppression, whereas the injection of splenic DCs from naive mice that were cocultured with OVA in vitro did not. These data suggest that not only CD4+ T cells, but also CD11c+ DCs induced by Ag feeding are important for the active transfer of oral tolerance in this murine experimental model of asthma.
DOI	10.4049/jimmunol.176.3.1481
PMID	16424176