Decrease of CD93 expression on the human monocyte-like cell line U937 treated with anti-Fas monoclonal antibody

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抗Fasモノクローナル抗体処理単球系細胞株(U937)表面上の補体(C1q)レセプター(CD93)の発現を我々が開発したCD93モノクローナル抗体(医学生物学研究所で販売)とフローサイトメトリー法を用いて解析した。その結果、抗Fasモノクローナル抗体処理U937細胞はアポトーシスマーカーであるAPO2.7分子の発現を誘導すると共に、細胞表面上のCD93分子の発現を著明に低下させた。また、この発現低下は抗Fasモノクローナル抗体の処理時間に依存していた。以上の結果から、抗Fasモノクローナル抗体処理単球系細胞株(U937)はFas/Fas ligand(Fas/Fas L)システムを介したCD93分子の発現調節を考察する上で非常に有益な情報を提供するものと考えられる。

Human CD93, a receptor for complement component 1, subcomponent q (C1qRp), was shown to be selectively expressed by cells of a myeloid lineage, and was originally reported to be involved in the C1q-mediated enhancement of phagocytosis in innate and adaptive immune responses. The modulation of CD93 expression also has been investigated in various cells, in particular, in granulocytes and monocytes. However, its modulation in myeloid cells with apoptotic properties remains poorly understood. In this study, using flow cytometry and two types of CD93 monoclonal antibodies (mAbs), mNI- 11 and X-2, we demonstrated the modulation of CD93 expression on the human monocyte-like cell line (U937) treated with an anti-Fas mAb, a substance for induction of apoptosis through the Fas/Fas ligand (FasL) system. The U937 cells expressed an apoptosis-related molecule, APO 2.7 after treatment with the anti-Fas mAb, and the expression of CD93 defined by mNI-11 or X-2 mAb on these cells was dramatically decreased. Furthermore, the decrease of CD93 expression on the U937 cells treated with anti-Fas mAb occurred in a time-dependent manner. Taken together, theses findings suggest that the decrease of CD93 expression on the U937 cells treated with anti-Fas mAb would be a good model for analyzing immunological responses in myeloid cells with apoptotic properties under C1q and CD93 interactions.

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