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趋化因子灭活剂对免疫复合物诱导的炎症的抑制作用。

Suppression of immune complex-induced inflammation by the chemotactic factor inactivator.

作者信息

Johnson K J, Anderson T P, Ward P A

出版信息

J Clin Invest. 1977 May;59(5):951-8. doi: 10.1172/JCI108717.

DOI:10.1172/JCI108717
PMID:140184
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC372303/
Abstract

Small amounts (10(-10) mol) of purified human chemotactic factor inactivator (CFI) suppress leukocytic infiltration, permeability changes, and hemorrhage associated with acute immune complex-induced injury in rats. The reversed passive dermal Arthus reaction and acute immune complex-induced alveolitis in rats have served as the model systems of inflammation. The mechanism of inhibition does not appear to relate to interference with formation and deposition of immune complexes, or with fixation of complement in vitro or iv vivo. Human CFI inhibits in vitro the chemotactic activity generated in complement-activated rat serum. The inhibitory effects of human CFI are not seen if it is first heat inactivated. The data provide the first direct support for the conclusion that CFI has anti-inflammatory activity.

摘要

少量(10⁻¹⁰摩尔)纯化的人趋化因子灭活剂(CFI)可抑制与大鼠急性免疫复合物诱导损伤相关的白细胞浸润、通透性变化和出血。大鼠的反向被动皮肤Arthus反应和急性免疫复合物诱导的肺泡炎已作为炎症的模型系统。抑制机制似乎与干扰免疫复合物的形成和沉积,或体外或体内补体的固定无关。人CFI在体外抑制补体激活的大鼠血清中产生的趋化活性。如果人CFI先经热灭活,则看不到其抑制作用。这些数据为CFI具有抗炎活性这一结论提供了首个直接支持。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061a/372303/6273a8f289ba/jcinvest00653-0222-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061a/372303/72280d76759e/jcinvest00653-0220-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061a/372303/a7500f513112/jcinvest00653-0221-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061a/372303/6273a8f289ba/jcinvest00653-0222-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061a/372303/72280d76759e/jcinvest00653-0220-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061a/372303/a7500f513112/jcinvest00653-0221-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061a/372303/6273a8f289ba/jcinvest00653-0222-a.jpg

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引用本文的文献

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3
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本文引用的文献

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BOUND COMPLEMENT AND IMMUNOLOGIC INJURY OF BLOOD VESSELS.补体结合与血管的免疫损伤
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The role of polymorphonuclear leukocytes in the initiation and cessation of the Arthus vasculitis.多形核白细胞在阿瑟斯血管炎起始与终止过程中的作用。
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9
Antiinflammatory effects of endotoxin. Inhibition of rabbit polymorphonuclear leukocyte responses to complement (C5)-derived peptides in vivo and in vitro.内毒素的抗炎作用。体内和体外对兔多形核白细胞对补体(C5)衍生肽反应的抑制。
Am J Pathol. 1983 Dec;113(3):291-9.
10
Effect of chlorpromazine on the development of experimental glomerulonephritis and Arthus reaction.氯丙嗪对实验性肾小球肾炎及阿瑟反应发展的影响。
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J Exp Med. 1966 Aug 1;124(2):209-26. doi: 10.1084/jem.124.2.209.
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C5 chemotactic fragments produced by an enzyme in lysosomal granules of neutrophils.由中性粒细胞溶酶体颗粒中的一种酶产生的C5趋化片段。
J Immunol. 1970 Mar;104(3):535-43.
5
Defective regulation of inflammatory mediators in Hodgkin's disease. Supernormal levels of chemotactic-factor inactivator.霍奇金病中炎症介质调节缺陷。趋化因子灭活剂水平超常。
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Characterization of serum inhibitors of neutrophil chemotaxis associated with anergy.与无反应性相关的中性粒细胞趋化作用血清抑制剂的特性分析
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Acute immunologic pulmonary alveolitis.急性免疫性肺泡炎
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8
Biologic role of complement products. Complement-derived leukotactic activity extractable from lesions of immunologic vasculitis.补体产物的生物学作用。可从免疫性血管炎病变中提取的补体源性趋化活性。
J Immunol. 1972 May;108(5):1137-45.
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Immunologic tissue injury mediated by neutrophilic leukocytes.由嗜中性白细胞介导的免疫性组织损伤。
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Chemotactic factor inactivator in normal human serum.正常人血清中的趋化因子灭活剂。
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