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分泌型免疫球蛋白A诱导的中性粒细胞介导的细胞毒性

Neutrophil-mediated cytotoxicity induced by secretory IgA.

作者信息

Geffner J R, Minnucci F, Isturiz M A

机构信息

Seción Inmunología Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Buenos Aires, Argentina.

出版信息

Immunol Lett. 1990 May;24(2):113-6. doi: 10.1016/0165-2478(90)90021-h.

DOI:10.1016/0165-2478(90)90021-h
PMID:2162328
Abstract

Normal human neutrophils triggered by secretory IgA (sIgA) displayed low levels of cytotoxicity towards non-sensitized red blood cells. Catalase completely impaired this non-specific cytotoxicity (NSC), while superoxide dismutase (SOD) significantly enhanced it, suggesting a key role for hydrogen peroxide (H2O2) in the lysis of target cells. Three heme-enzyme inhibitors, sodium azide, sodium cyanide and 3-amino-1,2,4-triazole, did not decrease NSC, but significantly enhanced it, suggesting that the mechanism involved is not dependent upon myeloperoxidase (MPO). Heat-aggregated IgG (HA-IgG) synergize with sIgA in promoting NSC. It was also found that gamma interferon significantly enhanced neutrophil-mediated NSC induced by sIgA, its effect being more dramatic on NSC triggered by low concentrations of sIgA. The significance of these results is discussed.

摘要

分泌型IgA(sIgA)触发的正常人中性粒细胞对未致敏红细胞表现出低水平的细胞毒性。过氧化氢酶完全削弱了这种非特异性细胞毒性(NSC),而超氧化物歧化酶(SOD)则显著增强了它,这表明过氧化氢(H2O2)在靶细胞裂解中起关键作用。三种血红素酶抑制剂,叠氮化钠、氰化钠和3-氨基-1,2,4-三唑,并没有降低NSC,反而显著增强了它,这表明所涉及的机制不依赖于髓过氧化物酶(MPO)。热聚集IgG(HA-IgG)在促进NSC方面与sIgA协同作用。还发现γ干扰素显著增强了sIgA诱导的中性粒细胞介导的NSC,其对低浓度sIgA触发的NSC的作用更为显著。讨论了这些结果的意义。

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