休克时白细胞表面LFA-1的表达

本实验以烫伤和创伤休克为模型，用单克隆抗体间接免疫荧光标记法对休克时白细胞表面LFA－1的表达进行了研究。结果烫伤及创伤休克白细胞表面LFA－1表达无增加甚至减少，提示LFA－1表达数量变化不是介导休克时白细胞粘附及渗出的主要原因。     

胶体金标记法测定创伤性休克时PMNs表面LFA-1的表达

目的研究创伤性休克时多形核粒细胞（ｐｏｌｙｍｏｒｐｈｏｎｕｃｌｅａｒ ｌｅｕｋｏｃｙｔｅｓ,ＰＭＮｓ）表面ＬＦＡ－１的表达情况。方法间接免疫胶体金标记法。结果创伤后ＰＭＮｓ表面及细胞内胶体金颗粒数明显减少（Ｐ<０ ．０１）。单位细胞体积所含有的金颗粒粒子数（个／μｍ３）,由正常对照组的３２４±１９,减至创伤组的７６±１５。结论在休克的发展中,白细胞表面ＬＦＡ－１表达量可能不是介导白细胞与内皮细胞粘附的主要原因。     

创伤性休克病人粒细胞表面Mac－1、CD18的表达

本研究用单克隆抗体间接免疫荧光标记法测定了创伤性休克时，多形核粒细胞（ｐｏｌｙ一ｍｏｒｐｈｏｎｕｃｌｅａｒｌｅｕｋｏｃｙｔｅｓ，ＰＭＮｓ）表面Ｍａｃ一１、ＣＤ１８的表达。结果表明，创伤后ＰＭＮｓ表面Ｍａｃ一１和ＣＤ１８表达有下调趋势。     

创伤性休克病人粒细胞表面Mac—1,CD18的表达

本研究用单克隆抗全间接免疫荧光标记测定了创伤性休克时，多形核粒细胞（ｐｏｌｙｍｏｒｐｈｏｎｕｃｌｅａｒｌｅｕｋｏｃｙｔｅｓ，ＰＭＮｓ）表面Ｍａｃ－１，ＣＤ１８的表达，结果表明，创伤后ＰＭＮｓ表面Ｍａｃ－１和ＣＤ１８表达有下调趋势。     

创伤性休克病人单个核细胞表面Mac─1、CD18的表达

用单克隆抗体间接免疫荧光标记法测定创伤性休克病人单个核细胞表面Ｍａｃ－１、ＣＤ１８的表达。结果，创伤后单个核细胞表面Ｍａｃ－１、ＣＤ１８表达增加，以ＣＤ１８为著。它可能参与休克时微循环中白细胞贴壁粘着的发生，带来微循环血流紊乱     

创伤性休克病人单个核细胞表面Mac─1、CD18的表达

用单克隆抗体间接免疫荧光标记法测定创伤性休克病人单个核细胞表面Ｍａｃ－１、ＣＤ１８的表达。结果，创伤后单个核细胞表面Ｍａｃ－１、ＣＤ１８表达增加，以ＣＤ１８为著。它可能参与休克时微循环中白细胞贴壁粘着的发生，带来微循环血流紊乱     

休克时白细胞表面ICAM—1的表达

目的：为探讨休克时白细胞膜表面ＩＣＡＭ－１的变化。方法：以烧伤和创伤休克为模型，用单克隆抗体间接免疫荧光标记法对休克时白细胞表面ＩＣＡＭ－１的表达。结果：烧伤及创伤后白细胞表面ＩＣＡＭ－１表达未见增多。结论：ＩＣＡＭ－１自白细胞膜脱落可能是其主要原因     

创伤性休克大鼠外周血白细胞表面LFA—1、ICAM—1表达的研究

自 198 1年发现ＣＤ11ａ/ＣＤ18,1986年发现不同于ＬＦＡ 1的细胞间粘附分子 (ｉｎｔｅｒｃｅｌｌｕｌａｒａｄｈｅｓｉｏｎｍｏｌｅｃｕｌｅ ,ＩＣＡＭ 1,亦名ＣＤ54,是ＬＦＡ 1的一种可诱导的细胞表面配基 )以来。人们对ＬＦＡ 1、ＩＣＡＭ 1的了解日益增多 ,并发现它们在细胞粘附中作用特别活跃。而有关创伤性休克时白细胞表面ＬＦＡ 1、Ｉ ＣＡＭ 1表达情况少见报道 ,故我们设计此实验以探讨创伤性休克时白细胞表面ＩＦＡ 1、ＩＣＡＭ 1的表达变化。1　材料与方法1 1　材料　取雄性ＳＤ大鼠 8只 ,体重 2 10～ 2 50ｇ ,随机分为 2组 :正…     

犬急性冠状动脉血栓时血小板膜糖蛋白CD62P和CD63的表达

目的：探讨犬急性冠状动脉血栓模型中血小板膜糖蛋白CD62P和CD63的阳性表达水平。方法：开胸微电流刺激麻醉犬左冠状动脉前降支血管外膜方法制备犬急性冠状动脉血栓模型，采用流式细胞仪和全血单克隆抗体直接免疫荧光标记法，对其血小板表面CD62P和CD63的表达进行检测。结果：8只犬制成犬急性冠状动脉血栓及急性心肌梗塞模型，其血小板表面CD62P和CD63阳性表达率分别为(36.2 4±11.69)%和(3.2 2±1.07)%，显著高于模型复制前基础值(8.35±2.73)%和(0.45±0.23)%（P<0.05）。结论：犬急性冠状动脉血栓模型中存在明显的血小板活化现象，血小板膜糖蛋白CD62P和CD63的表达率显著升高     

KIM185, a monoclonal antibody to CD18 which induces a change in the conformation of CD18 and promotes both LFA-1- and CR3-dependent adhesion

Unactivated peripheral blood leukocytes show little tendency to bind to other cells or matrix components, whilst, in the presence of inflammatory mediators, adhesive interactions can rapidly increase. The Leu-CAM (β₂ integrin) family of adhesion molecules have been shown to mediate a variety of these induced adhesion events. Here we describe a monoclonal antibody against CD18, KIM185, which stimulates JY cell homotypic aggregation by a CD11a pathway as well as inducing the adherence of neutrophils to protein-coated plastic by a CD lib-dependent mechanism. The antibody recognizes an epitope distinct from the previously described KIM127 antibody and evidence is presented that the binding of KIM185 can cause a change in the conformation of the CD18 molecule.     

Characterization of four CD18 mutants in leucocyte adhesion deficient (LAD) patients with differential capacities to support expression and function of the CD11/CD18 integrins LFA-1, Mac-1 and p150,95.

Leucocyte adhesion deficiency (LAD) is a hereditary disorder caused by mutations in the CD18 (beta2 integrin) gene. Four missense mutations have been identified in three patients. CD18(A270V) supports, at a diminished level, CD11b/CD18 (Mac-1, alphaMbeta2 integrin) and CD11c/CD18 (p150,95, alphaXbeta2 integrin) expression and function but not CD11a/CD18 (LFA-1, alphaLbeta2 integrin) expression. Conversely, CD18(A341P) supports a limited level of expression and function of CD11a/CD18, but not of the other two CD11/CD18 antigens. CD18(C590R) and CD18(R593C) show a decreasing capacity to associate with the CD11a, CD11c and CD11b subunits. Transfectants expressing the CD11a/CD18 with the C590R and R593C mutations are more adhesive than transfectants expressing wild-type LFA-1, and express the reporter epitope of the monoclonal antibody 24 constitutively. Thus, the four mutations affect CD18 differently in its capacities to support CD11/CD18 expression and adhesion. These results not only provide a biochemical account for the clinical diversity of patients with leucocyte adhesion deficiency, but also offer novel insights into the structural basis of interaction between the alpha and beta subunits, which is an integral component in our understanding of integrin-mediated adhesion and its regulation.     

Distinct Kinetics Features of LFA-1 and Mac-1 in Neutrophil Activation

LFA-1 and Mac-l, two [32 integrin members constitutively expressed on neutrophils, mediate leukocyte recruitment cascade by binding to the same ligand of ICAM-1. The slow rolling and firm adhesion of leukoeytes rely on LFA-1 while the cell crawling is dependent on Mac-1. We hypothesized that their distinct roles were likely attributed to the differences in the binding kinetics or in the diverse responses of outside-in and inside-out signaling. In this study, we compared the ICAM-1 binding features between soluble or membrane-expressed LFA-1 and Mac-1 with different affinity conformations using optical trap technique. Our data indicate that the affinity up-regulation from wide type （WT） to high affinity （HA） is off-rate dependent for LFA-1 but on-rate dependent for Mac-1. The structural bases of this new finding were found to be consistent with our previous simulations. These results furthered our understanding on their function differences under shear flow.     

Distinct Kinetics Features of LFA-1 and Mac-1 in Neutrophil Activation

LFA-1 and Mac-1, two β2integrin members constitutively expressed on neutrophils, mediate leukocyte recruitment cascade by binding to the same ligand of ICAM-1. The slow rolling and firm adhesion of leukocytes rely on LFA-1 while the cell crawling is dependent on Mac-1. We hypothesized that their distinct roles are likely attributed to the differences in the binding kinetics or in the diverse responses of outside-in and inside-out signaling. In this study, we compared the ICAM-1 binding features between soluble or membrane-expressed LFA-1 and Mac-1 with different affinity conformation using optical trap technique. Our data indicated that the affinity up-regulation from wide type(WT) to high affinity(HA) is off-rate dependent for LFA-1but on-rate dependent for Mac-1. The structural bases of this new finding were found to be consistent with our previous simulations. These results furthered our understanding in their function differences under shear flow.