リンパ球に発現している新しい接着因子の同定と解析

淋巴细胞表达的新粘附因子的鉴定和分析

• 批准号: 04454571
• 负责人: 内山 卓
• 金额: $ 3.33万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1992
• 资助国家: 日本
• 起止时间: 1992 至 无数据
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04454571/
• 关键词: 細胞接着因子; ATL; HTLV-1

正常リンパ球と血管内皮細胞との接着に関与していると考えられる既知のLFA-1,VLA-4,糖鎖抗原(sLe^a,sLe^x),CD44,LECAM1などの接着以外の接着因子を,10例のATL患者白血病細胞,10株のHTLV-I感染T細胞株を用いて,^<51>Cr標識細胞と臍帯静脈由来血管内皮細胞(HUVEC)との接着現象の系で検索した。フローサイトメトリー解析では,半数以上の症例,細胞株でLFA-1,VLA-4,CD44,LECAM1,sLe^xの発現が認められた。非刺激HUVECに対しては,10例中1例,10株中9株で,IL-1刺激後HUVECに対しては,全例全株で明らかな接着がみられた。各種接着因子に対する抗体を用いた接着阻止実験で次の結果を得た。1.ATL患者白血病細胞はELAM1を介する接着が,HTLV-1感染細胞株ではELAM1および,一部VLA-4を介する接着が主要である。2.しかし,LFA-1,VLA-4,ELAM1すべてに対する抗体によっても阻止できない接着が明らかに存在する。3.一方,対照とした健常人末梢血CD4^+CD45RO^+T細胞では,非刺激HUVECにはほとんど接着しないが,PMA刺激HUVECには50-80%の接着を示し,この接着はLFA-1,VLA-4,ELAM1抗体の同時添加でほぼ完全に阻止される。4.HTLV-1非感染T細胞株(6株)でのIL-1刺激HUVECへの接着は,既知3接着因子に対する抗体で完全に阻止される。すなわち,ATL患者白血病細胞,HTLV-1感染T細胞株は,ELAM1を介する接着が主要なものであるが,これ以外の未知のHUVECとの接着を来たす因子の存在することが強く示唆される結果を得た。この結果をもとにして,HUVECへの接着阻止を指標に,未知接着因子に対する抗体の作製を試みたが,本年度は成功しなかった。

LFA-1,VLA-4, glycogen antigen (SLE ^ a, SLE ^ x), CD44,LECAM1 antigen (SLE ^ a, SLE ^ x), leukemic cells from 10 patients with HTLV-I and 10 T cell lines infected with HTLV-I were tested. The Cr tag identifies the origin of the vascular endothelial cell (HUVEC) as the origin of the vascular endothelial cell and then the image of the cord. In more than half of the cases, the cell line LFA-1 was found to be LFA-1, and the cell line LFA-1, VLARICE 4, CD44, LECAM1, sle ^ x, LFA-1, CD44, LFA-1, LFA-1, Unstimulated HUVEC infected mice, 1 out of 10 cases, 9 strains out of 10 strains. After IL-1 stimulation, HUVEC strains were infected, and in all cases, the whole plant was infected. A variety of subsequent factors were used to detect antibodies and then to prevent secondary tests. The leukemic cells of 1.ATL patients were divided into two groups: ELAM1, HTLV-1 infection, ELAM1 infection, and one VLA-4 intervention followed by primary infection. two。 The antibody was blocked by LFA-1,VLA-4,ELAM1, and then the presence of antibody was detected. 3. On the one hand, according to the normal person peripheral blood CD4 ^ + CD45RO^ + T cell cycle, non-stimulated HUVEC response followed by stimulation, PMA stimulation of HUVEC 50-80% followed by warning, then LFA-1,VLA-4,ELAM1 antibody was added at the same time to completely stop the infection. 4.HTLV-1 non-infected T cell lines (6 strains) were stimulated by IL-1 to stimulate HUVEC infection, and it was known that the antibody could completely block the infection. The leukemic cells of patients with ATL were infected with HTLV-1, and the T cell line was infected by HTLV-1. The main infection was followed by the introduction of ELAM1, and the presence of unknown HUVEC in the presence of other factors. The results show that the HUVEC will then block the finger, and the unknown factor will be followed by the antibody. This year, we have succeeded in this year.