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系统性红斑狼疮中补体(C5)衍生趋化活性的特异性抑制剂,在抗原性上与人B因子的Bb片段相关。

Specific inhibitor of complement (C5)-derived chemotactic activity in systemic lupus erythematosus related antigenically to the Bb fragment of human factor B.

作者信息

Perez H D, Hooper C, Volanakis J, Ueda A

出版信息

J Immunol. 1987 Jul 15;139(2):484-9.

PMID:3648093
Abstract

Serum and plasma from patients with active systemic lupus erythematosus contain a specific inhibitor of complement (C5)-derived chemotactic activity. We found that the inhibitor is antigenically related to the Bb fragment of complement factor B. Lupus plasma and purified inhibitor significantly reduced the chemotactic activity of zymosan-treated normal serum, an effect that was abolished by antibodies to factor B. Similar results were obtained when purified Bb was used. Neither purified inhibitor nor Bb inhibited the chemotactic activity of purified human C5a or C5a des Arg. As reported previously, the chemotactic activity of C5a des Arg was enhanced significantly by the addition of an anionic polypeptide (cochemotaxin) present in normal serum and plasma. Interestingly, both purified lupus inhibitor and Bb inhibited the chemotactic activity exhibited by mixtures of C5a des Arg and its cochemotaxin. This effect was due, most likely, to their ability to neutralize the enhancing effect of the cochemotaxin on the chemotactic activity of C5a des Arg. Immunoelectrophoresis and western blots revealed that the purified inhibitor reacted with anti-factor B and exhibited a similar charge and molecular weight as purified Bb.

摘要

活动性系统性红斑狼疮患者的血清和血浆中含有一种补体(C5)衍生趋化活性的特异性抑制剂。我们发现该抑制剂与补体因子B的Bb片段存在抗原相关性。狼疮血浆和纯化的抑制剂显著降低了经酵母聚糖处理的正常血清的趋化活性,抗因子B抗体可消除这一效应。使用纯化的Bb时也得到了类似结果。纯化的抑制剂和Bb均未抑制纯化的人C5a或C5a去精氨酸的趋化活性。如先前报道,正常血清和血浆中存在的一种阴离子多肽(共趋化因子)可显著增强C5a去精氨酸的趋化活性。有趣的是,纯化的狼疮抑制剂和Bb均抑制了C5a去精氨酸与其共趋化因子混合物所表现出的趋化活性。这种效应很可能是由于它们能够中和共趋化因子对C5a去精氨酸趋化活性的增强作用。免疫电泳和western印迹显示,纯化的抑制剂与抗因子B发生反应,且所带电荷和分子量与纯化的Bb相似。

相似文献

1
Specific inhibitor of complement (C5)-derived chemotactic activity in systemic lupus erythematosus related antigenically to the Bb fragment of human factor B.系统性红斑狼疮中补体(C5)衍生趋化活性的特异性抑制剂,在抗原性上与人B因子的Bb片段相关。
J Immunol. 1987 Jul 15;139(2):484-9.
2
Polymorphonuclear leukocyte chemotaxis in systemic lupus erythematosus.系统性红斑狼疮中的多形核白细胞趋化作用。
J Rheumatol Suppl. 1987 Jun;14 Suppl 13:53-8.
3
A specific inhibitor of complement (C5)-derived chemotactic activity in serum from patients with systemic lupus erythematosus.系统性红斑狼疮患者血清中补体(C5)衍生趋化活性的特异性抑制剂。
J Clin Invest. 1978 Jul;62(1):29-38. doi: 10.1172/JCI109110.
4
Enhancement of the chemotactic activity of human C5a des Arg by an anionic polypeptide ("cochemotaxin") in normal serum and plasma.正常血清和血浆中一种阴离子多肽(“协同趋化因子”)增强人C5a去精氨酸的趋化活性。
J Immunol. 1981 Feb;126(2):800-4.
5
Attachment of human C5a des Arg to its cochemotaxin is required for maximum expression of chemotactic activity.人C5a去精氨酸产物与共趋化因子结合对于趋化活性的最大表达是必需的。
J Clin Invest. 1986 Dec;78(6):1589-95. doi: 10.1172/JCI112751.
6
Human C5a and C5a des Arg exhibit chemotactic activity for fibroblasts.人C5a和C5a去精氨酸对成纤维细胞表现出趋化活性。
J Immunol. 1988 Nov 15;141(10):3570-4.
7
Group B streptococci inhibit the chemotactic activity of the fifth component of complement.B族链球菌抑制补体第五成分的趋化活性。
J Immunol. 1988 Nov 15;141(10):3551-6.
8
Role of chemotactic factor inactivator in modulating alveolar macrophage-derived neutrophil chemotactic activity.趋化因子灭活剂在调节肺泡巨噬细胞衍生的中性粒细胞趋化活性中的作用。
J Lab Clin Med. 1987 Feb;109(2):164-70.
9
Chemotactic peptides modulate adherence of human polymorphonuclear leukocytes to monolayers of cultured endothelial cells.趋化肽可调节人类多形核白细胞对培养的内皮细胞单层的黏附。
J Immunol. 1986 May 1;136(9):3412-9.
10
Chemotactic responses of human peripheral blood monocytes to the complement-derived peptides C5a and C5a des Arg.人外周血单核细胞对补体衍生肽C5a和C5a去精氨酸的趋化反应。
J Immunol. 1985 May;134(5):3325-31.

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Infection with Opportunistic Bacteria Triggers Severe Pulmonary Inflammation in Lupus-Prone Mice.机会性细菌感染引发狼疮易感小鼠严重肺部炎症。
Mediators Inflamm. 2019 Sep 3;2019:1701367. doi: 10.1155/2019/1701367. eCollection 2019.
2
Infectious diseases associated with complement deficiencies.与补体缺陷相关的传染病。
Clin Microbiol Rev. 1991 Jul;4(3):359-95. doi: 10.1128/CMR.4.3.359.