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Margaret J. Tango Evelyn Safaris Margarita Romanella Atousa Aminian Marina Katerelos Christine Somerwille RIek G. Tearle Martin J. Pearse Anthony J.E d'Apice 《Xenotransplantation》1997,4(1):25-33
Abstract: Transgenic expression of the human complement regulatory molecule CD59 in mice and genetic deletion of the major xenoantigen galactose α 1,3 galactose (Gal KO) each resulted in partial protection of spleen cells from lysis by human serum. These protective effects were additive when the two genetic modifications were combined. However, when the effects of these genetic modifications were examined in an ex vivo model in which mouse hearts were perfused with human plasma, it was Gal KO which was the modification which determined protection. CD59 expression alone was not protective and CD59 expression in combination with Gal knockout did not result in a significant additional increase in protection over and above that provided by Gal knockout alone. The likely explanation for this discrepancy between the in vitro and ex vivo data is that the H2-Kb promoter used to drive CD59 expression results I in substantially less expression on endothelium than on spleen cells. 相似文献
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目的 研究不同透析膜对维持性血液透析 (MHD)患者外周血转化生长因子 β1及补体调节蛋白CD5 9活性表达的影响。方法 通过流式细胞术和酶联免疫吸附法测定长期采用铜仿膜 (CU)与聚砜膜 (PSU)透析患者外周血TGF β1水平及CD5 9活性表达。结果 MHD患者血浆TGF β1水平明显增加 (P <0 .0 5 ) ,其中CU组为 (81.7± 8.7)ng mL ;PSU组为 (6 4 .3±8.3)ng mL ,与正常对照组 (49.3± 6 .1)ng mL相比均有显著差异 (P <0 .0 1,P <0 .0 5 ) ;而PSU组与CU组相比 ,外周血TGF β1水平明显下降 (P <0 .0 5 )。CD5 9在正常人外周血单个核细胞中无表达 ,而在尿毒症未透析组及血透组均有表达 ,其中未透析组表达较低 ,而血透组表达较高 ,CU膜血透组较PSU血透组表达要高 (P <0 .0 5 )。经相关分析结果显示 :CU组与PSU组内TGF β1水平与CD5 9表达均呈现良好的相关性 (r=0 .6 4 0 9与 0 .5 83,P <0 .0 5 )。 结论 血液透析通过血液 透析膜间相互反应可活化补体 ,诱导外周血单个核细胞 (PBMC)合成TGF β1增多 ,而增高的TGF β1水平可上调CD5 9基因表达 ,抑制补体异常活化造成的细胞破坏 ,对机体具有代偿性保护意义。然而不同透析膜如CU和PSU对MHD患者TGF β1与CD5 9的影响有所不同 ,这些变化与透析膜的生物相容性有关 相似文献
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Varsano Rashkovsky Shapiro Ophir Mark-Bentankur 《Clinical and experimental immunology》1998,113(2):173-182
Human lung cancer expresses cell membrane complement inhibitory proteins (CIP). We investigated whether human lung cancer cell lines also express cell-membrane CIP molecules and whether the biology of CIP molecules in these cell lines differs from that of CIP in normal human respiratory epithelium in culture. The cell lines ChaGo K-1 and NCI-H596 were compared with normal human nasal epithelium in primary cultures in respect to the level of cell membrane CIP expression of membrane cofactor protein (MCP; CD46), decay-accelerating factor (DAF; CD55) and CD59, in respect to the level of cell resistance to complement-mediated lysis, and in respect to the contribution of cell membrane CIP to cell resistance against complement-mediated lysis. We found, using flow cytometry, that both human lung cancer cell lines expressed MCP, DAF and CD59, as did normal nasal epithelial cells. However, normal cells showed a large subpopulation of low DAF-expressing cells (60% of all cells) and a smaller subpopulation of high DAF-expressing cells (40%), while the lung cancer cell lines showed only one cell population, of high DAF expression. In addition, both lung cancer cell lines expressed higher MCP levels, and NCI-H596 cells showed higher levels of CD59. Cell resistance to complement-mediated lysis of both lung cancer cell lines was much higher than that of normal cells. Fifty percent normal human serum, under the same concentrations of complement activators, induced lysis of less than a mean of 10% of lung cancer cells, while lysing up to a mean of 50% of nasal epithelial cells. Lung cancer cell resistance to complement was due to its ability to prevent significant activation of complement upon its cell membrane, as manifested by a failure of complement activators to increase cell membrane deposition of C3-related fragments. The exact mechanism for this resistance remains obscure. Unexpectedly, neutralizing antibodies, anti-MCP and anti-DAF were entirely ineffective and anti-CD59 was only slightly effective (18% mean cell lysis) in increasing the susceptibility of the lung cancer cell lines to complement, while the same antibodies were very effective in facilitating complement-mediated lysis of the normal nasal epithelial cells (50% mean cell lysis with CD59 MoAb). On the other hand, detachment of DAF and CD59 by phosphatidylinositol-specific phospholipase C (PIPLC) from the lung cancer cell lines abrogated their resistance to lysis. We suggest that the biology of cell membrane CIP molecules in human lung cancer cell lines is different from that of CIP in normal respiratory epithelial cells. Human lung cancer cell lines are able to prevent significant complement activation upon its cell membrane and are therefore especially resistant to complement-mediated lysis. Complement resistance may serve this common and highly lethal human cancer as an escape mechanism from the body's immunosurveillance and prevent effective immunotherapy with tumour-specific MoAbs. 相似文献
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用抗CD59单抗2A7与CNBr-Sepharose4B偶联制备亲和层析柱,从正常人红细胞膜蛋白抽提物中分离纯化出CD59分子。本法纯化的CD59分子量为18-20KDa对还原剂敏感,与McAbssMEM43和1F5有高亲和性,再掺入豚鼠红细胞后,能够抑制人体补体的反应性溶血,本文还对三株抗CD59单抗2A7,MEM43及1F5的抗原特异性进行了初步分析。 相似文献
8.
Membrane attack complex of complement and 20 kDa homologous restriction factor (CD59) in myocardial infarction 总被引:4,自引:0,他引:4
Toyohiro Tada Hidechika Okada Noriko Okada Hisashi Tateyama Harumi Suzuki Youhei Takahashi Tadaaki Eimoto 《Virchows Archiv : an international journal of pathology》1997,430(4):327-332
In order to investigate the mechanism of deposition of the complement membrane attack complex (MAC) in cardiomyocytes in areas of human myocardial infarction, the 20 kDA homologous restriction factor of complement (HRF20; CD59) and complement components (C1q, C3d and MAC) were analysed immunohistochemically using specific antibodies. Myocardial tissues obtained at autopsy from nine patients who died of acute myocardial infarction were fixed in acetone and embedded in paraffin. The ages of the infarcts ranged from about 3.5 h to 12 days. In cases of myocardial infarction of 20 h or less, MAC deposition was shown in the infarcted cardiomyocytes without loss of HRF20. Where the duration was 4 days or more, the cardiomyocytes with MAC deposition in the infarcted areas also showed complete loss of HRF20. Outside the infarcts, HRF20 in the cardiomyocytes was well preserved without MAC deposition. The present study suggests that the initial MAC deposition in dead cardiomyocytes can occur as a result of degradation of plasma-membrane by a mechanism independent of complement-mediated injury to the membrane. Loss of HRF20 from dead cardiomyocytes may not be the initial cause of MAC deposition, but may accelerate the deposition process of MAC in later stages of infarction. 相似文献
9.
Anne Marie-Cardine Henning Kirchgessner Christoph Eckerskorn Stefan C. Meuer Burkhart Schraven 《European journal of immunology》1995,25(12):3290-3297
A glutathione-S-transferase-src-homology domain 2 (GST-SH2) fusion protein was employed to identify molecules interacting with the protein tyrosine kinase p59fyn. Among several proteins which bound to the fyn SH2 domain in lysates of human Jurkat T lymphocytes, α- and β-tubulin were identified by N-terminal sequencing. Further analysis established that α-tubulin exists as a tyrosine-phosphorylated protein in Jurkat cells, where it interacts with p59fyn, but not with p56lck. By contrast, in untransformed resting human T lymphocytes α-tubulin is not detectable as a tyrosine phosphorylated protein. However, following T cell activation, it becomes rapidly phosphorylated on tyrosine residues and subsequently associates with the SH2 domain of fyn. Interestingly, constitutively tyrosine-phosphorylated α-tubulin that is able to interact with the fyn-SH2 domain is expressed in peripheral blood T lymphoblasts isolated from leukemic patients in the absence of external stimulation. 相似文献
10.
The effect of adrenergic and cholinergic drugs on short incubation “active” E rosette formation was studied in 19 patients with bronchial asthma and 17 healthy controls. Both groups had an equal absolute number of baseline “active” E rosettes, but the asthmatics demonstrated a higher percent baseline value. The beta adrenergic drug isoproterenol (10?3 M) inhibited the formation of “active” E rosettes in asthmatics by only 18.0% as compared to a 60.8% inhibition in the control group. Carbamylcholine (10?5 M) a cholinergic agonist, also showed a lower than normal response in asthmatics, 34.3% enhancement of “active” E rosetting compared to a 52.4% enhancement in the controls. The alpha adrenergic agent phenylephrine (10?5 M) exhibited equal enhancing effects in both groups, 34.2% in the asthmatics and 36.5% in the controls. Isoproterenol (10?3 M) had a minimal effect on inhibition of long incubation “total” E rosettes in both groups studied. The beta adrenergic abnormality conforms to the beta blockade theory of asthma of Szentivanyi. The cholinergic abnormality is unexplained in view of the hyperresponsiveness of patients with asthma to cholinergic agents in vivo. Patients with bronchial asthma probably have an autonomic dysfunction that may play a role in the pathogenesis of their disease. 相似文献