上海医科大学学报
上海醫科大學學報
상해의과대학학보
JOURNAL OF SHANGHAI MEDICAL UNIVERSITY
2000年
6期
431-434
,共4页
刘村兰%石原克彦%平野俊夫
劉村蘭%石原剋彥%平野俊伕
류촌란%석원극언%평야준부
抗人BST-1多克隆抗体%髓系细胞%酪氨酸磷酸化
抗人BST-1多剋隆抗體%髓繫細胞%酪氨痠燐痠化
항인BST-1다극륭항체%수계세포%락안산린산화
anti-human BST-1 polyclonal antibody%myeloid cells%tyrosine phosphorylation
目的探讨髓系细胞表面BST-1(骨髓基质细胞抗原1)/CD157分子能否作为一受体介导信号传导和调节细胞表面FcγR的表达。方法制备兔抗人BST-1多克隆抗体及其F(ab')2片段,以其刺激U937细胞后,用免疫沉淀及免疫印迹法研究胞内蛋白酪氨酸磷酸化水平的变化;用FACS法检测细胞表面FcγR的表达。结果抗人BST-1抗体刺激U937细胞可介导胞内多种蛋白的酪氨酸磷酸化水平增高,包括Mr为120×103的c-cbl原癌蛋白;并可下调细胞表面CD64的表达。抗BST-1抗体的这些作用呈抗体Fc段依赖性。结论髓系细胞表面BST-1分子可作为一受体介导细胞信号传导;抗BST-1抗体刺激U937细胞可下调其表面CD64的表达
目的探討髓繫細胞錶麵BST-1(骨髓基質細胞抗原1)/CD157分子能否作為一受體介導信號傳導和調節細胞錶麵FcγR的錶達。方法製備兔抗人BST-1多剋隆抗體及其F(ab')2片段,以其刺激U937細胞後,用免疫沉澱及免疫印跡法研究胞內蛋白酪氨痠燐痠化水平的變化;用FACS法檢測細胞錶麵FcγR的錶達。結果抗人BST-1抗體刺激U937細胞可介導胞內多種蛋白的酪氨痠燐痠化水平增高,包括Mr為120×103的c-cbl原癌蛋白;併可下調細胞錶麵CD64的錶達。抗BST-1抗體的這些作用呈抗體Fc段依賴性。結論髓繫細胞錶麵BST-1分子可作為一受體介導細胞信號傳導;抗BST-1抗體刺激U937細胞可下調其錶麵CD64的錶達
목적탐토수계세포표면BST-1(골수기질세포항원1)/CD157분자능부작위일수체개도신호전도화조절세포표면FcγR적표체。방법제비토항인BST-1다극륭항체급기F(ab')2편단,이기자격U937세포후,용면역침정급면역인적법연구포내단백락안산린산화수평적변화;용FACS법검측세포표면FcγR적표체。결과항인BST-1항체자격U937세포가개도포내다충단백적락안산린산화수평증고,포괄Mr위120×103적c-cbl원암단백;병가하조세포표면CD64적표체。항BST-1항체적저사작용정항체Fc단의뢰성。결론수계세포표면BST-1분자가작위일수체개도세포신호전도;항BST-1항체자격U937세포가하조기표면CD64적표체
Purpose To examine whether BST-1/CD157 expressed on myeloid cells can function as a receptor molecule to mediate signal into cells and regulate the expression of FcγR on cells. Methods The tyrosine phosphorylation of U937 cells stimulated by immunoprecipitation and immunoblotting method;FcγR expression level on U937 cells stimulated by anti-BST-antibody was analyzed by FACS. Results Stimulation of U937 cells by anti-BST-1 polyclonal antibody resulted in protein tyrosine phosphorylation of U937 cells,including Mr 120×103 c-cbl onco-protein,and the down-regulation of CD64 expression on U937 cells.The activities of anti-BST-1 antibody depended on its Fc portion. Conclusions BST-1 molecules expressed on myeloid cells can function as a receptor molecule to mediate signal into cells.Stimulation of U937 cells by anti-BST-1 antibody down-regulate the expression of CD64.