@article{oai:phoenix.repo.nii.ac.jp:00000947,
 author = {池脇, 信直 and Ikewaki, Nobunao and 園田, 徹 and 右田, 平八 and イケワキ, ノブナオ and ソノダ, トオル and ミギタ, ヘイハチ and IKEWAKI, Nobunao and SONODA, Tohru and MIGITA, Heihachi},
 journal = {九州保健福祉大学研究紀要, Journal of Kyushu University of Health and Welfare},
 month = {Mar},
 note = {P(論文), ニッケルで処理されたヒト単球系細胞株(U937)におけるCD93 分子の動態を解析した。ニッケル処理はU937 細胞に対してインターロイキン-8(IL-8) の産生を増強しながらアポトーシスを誘導した。また、ニッケル処理によりU937 細胞表面上のCD93 分子(mCD93)の発現は有意に減少し、可溶性CD93 分子(sCD93)の産生は有意に増強した。以上の結果は、CD93 分子の動態が金属(ニッケル)アレルギーの発症メカニズムを解析するための新たなバイオマーカーに成り得ることを示唆している。, In this study, we demonstrated the modulation of CD93 molecules (both membrane-bound and soluble-form) in a human monocyte-like cell line, U937 treated with nickel (Ni2+) to model contact hypersensitivity (CHS), such as metal allergy. Ni2+ induced the apoptosis of the U937 cells accompanied by the enhanced secretion of an inflammatory cytokine, interleukin-8 (IL-8). The percentages and mean fluorescence intensities (MFIs) of membrane-bound CD93 (mCD93) expressed on U937 cells were significantly decreased after treatment with Ni2+ when examined using flow cytometry with a CD93 monoclonal antibody (mAb) (mNI-11), which was established in our laboratories. In contrast, the secretion of soluble-form CD93 (sCD93) from U937 cells increased markedly after treatment with Ni2+. Taken together, these findings suggest that the modulation of CD93 molecules (both mCD93 and sCD93) might serve as a new biomarker for analyzing the inflammatory reaction in CHS induced by Ni2+.},
 pages = {129--137},
 title = {ニッケルで処理されたヒト単球系細胞株(U937)におけるCD93分子の動態},
 volume = {15},
 year = {2014},
 yomi = {イケワキ, ノブナオ and ソノダ, トオル and ミギタ, ヘイハチ}
}