急性疟疾患儿的补体激活
Complement activation in children with acute malaria.
作者信息
Greenwood B M, Brueton M J
出版信息
Clin Exp Immunol. 1974 Oct;18(2):267-72.
Abstract
Low C3 levels were found in the sera of most children with acute malaria. C4 and C1q levels were very low whilst glycine-rich β-glycoprotein (GBG) levels were only slightly depressed, suggesting that complement activation was occurring via the classical pathway. It is suggested that complement activation may play a part in initiating the complex series of changes that leads to the vascular damage seen in this infection.
摘要
在大多数急性疟疾患儿的血清中发现C3水平较低。C4和C1q水平非常低，而富含甘氨酸的β-糖蛋白（GBG）水平仅略有下降，这表明补体激活是通过经典途径发生的。有人认为，补体激活可能在引发导致这种感染中所见血管损伤的一系列复杂变化中起作用。
相似文献
1
Complement activation in children with acute malaria.急性疟疾患儿的补体激活
Clin Exp Immunol. 1974 Oct;18(2):267-72.
2
[Transitory deficiency of Clq and C4 in a case of chronic glomerulonephritis].
Minerva Nefrol. 1975 Nov-Dec;22(6):266-71.
3
[Complement system in glomerulonephritis. II. Detailed aspects].[肾小球肾炎中的补体系统。II. 详细方面]
Pediatr Pol. 1980 Jun;55(6):805-11.
4
5
Complement deficiency states.补体缺乏状态。
Medicine (Baltimore). 1978 Jan;57(1):1-23. doi: 10.1097/00005792-197801000-00001.
6
Inherited deficiencies of complement in man.人类补体的遗传性缺陷。
Int J Dermatol. 1977 Dec;16(10):775-92. doi: 10.1111/j.1365-4362.1977.tb04296.x.
7
The HLA system and inherited deficiencies of the complement system.HLA系统与补体系统的遗传性缺陷。
Transplant Rev. 1976;32:43-71. doi: 10.1111/j.1600-065x.1976.tb00228.x.
8
Genetic aspects of complement and glomerulonephritis.补体与肾小球肾炎的遗传学方面
Adv Nephrol Necker Hosp. 1984;13:271-96.
9
Genetic deficiencies of complement.补体的遗传缺陷
Ann Med. 1995 Aug;27(4):451-9. doi: 10.3109/07853899709002453.
10
Inherited complement component abnormalities.遗传性补体成分异常。
Annu Rev Med. 1986;37:333-46. doi: 10.1146/annurev.me.37.020186.002001.
引用本文的文献
1
Nonsynonymous amino acid changes in the α-chain of complement component 5 influence longitudinal susceptibility to infections and severe malarial anemia in kenyan children.补体成分5α链中的非同义氨基酸变化影响肯尼亚儿童对感染和严重疟疾贫血的长期易感性。
Front Genet. 2022 Sep 14;13:977810. doi: 10.3389/fgene.2022.977810. eCollection 2022.
2
Complement C1s cleaves PfEMP1 at interdomain conserved sites inhibiting cytoadherence.补体 C1s 在 PfEMP1 的结构域保守位点切割，抑制细胞黏附。
Proc Natl Acad Sci U S A. 2021 Jun 1;118(22). doi: 10.1073/pnas.2104166118.
3
Antibodies and Protection in Systemic Infections: Do We Still Have More Questions than Answers?全身性感染中的抗体和保护作用：我们是否仍有更多的疑问而非答案？
Infect Immun. 2020 Sep 18;88(10). doi: 10.1128/IAI.00219-20.
4
The Complement System Contributes to Functional Antibody-Mediated Responses Induced by Immunization with Plasmodium falciparum Malaria Sporozoites.补体系统有助于诱导对疟原虫疟原虫孢子的免疫接种产生功能性抗体介导的反应。
Infect Immun. 2018 Jun 21;86(7). doi: 10.1128/IAI.00920-17. Print 2018 Jul.
5
Immunological bases of increased susceptibility to invasive nontyphoidal Salmonella infection in children with malaria and anaemia.疟疾和贫血儿童对侵袭性非伤寒沙门氏菌感染易感性增加的免疫学基础。
Microbes Infect. 2018 Oct-Nov;20(9-10):589-598. doi: 10.1016/j.micinf.2017.11.014. Epub 2017 Dec 15.
6
The Plasmodium falciparum blood stages acquire factor H family proteins to evade destruction by human complement.恶性疟原虫血液阶段获取补体H因子家族蛋白以逃避人类补体的破坏。
Cell Microbiol. 2016 Apr;18(4):573-90. doi: 10.1111/cmi.12535. Epub 2015 Nov 12.
7
Complement activation by merozoite antigens of Plasmodium falciparum.恶性疟原虫裂殖子抗原激活补体。
PLoS One. 2014 Aug 21;9(8):e105093. doi: 10.1371/journal.pone.0105093. eCollection 2014.
8
Potential immune mechanisms associated with anemia in Plasmodium vivax malaria: a puzzling question.间日疟原虫疟疾中与贫血相关的潜在免疫机制：一个令人困惑的问题。
Infect Immun. 2014 Oct;82(10):3990-4000. doi: 10.1128/IAI.01972-14. Epub 2014 Aug 4.
9
Malaria parasite infection compromises control of concurrent systemic non-typhoidal Salmonella infection via IL-10-mediated alteration of myeloid cell function.疟原虫感染通过IL-10介导的髓样细胞功能改变，损害对同时发生的全身性非伤寒沙门氏菌感染的控制。
PLoS Pathog. 2014 May 1;10(5):e1004049. doi: 10.1371/journal.ppat.1004049. eCollection 2014 May.
10
Malarial pigment hemozoin and the innate inflammatory response.疟色素疟原虫色素与先天性炎症反应。
Front Immunol. 2014 Feb 5;5:25. doi: 10.3389/fimmu.2014.00025. eCollection 2014.
本文引用的文献
1
THE COMPLEMENT CONTENT OF HUMAN SERA WITH ESPECIAL REFERENCE TO MALARIA.人体血清中的补体含量，特别是与疟疾的关系
J Clin Invest. 1948 May;27(3 Pt 1):320-6. doi: 10.1172/JCI101960.
2
Blood coagulation initiation by a complement-mediated pathway.补体介导途径引发血液凝固。
J Exp Med. 1971 Dec 1;134(6):1601-7. doi: 10.1084/jem.134.6.1601.
3
Complement in acute experimental malaria. II. Alterations in the components of complement.
Mil Med. 1966 Sep;131(9):Suppl:1180-90.
4
Complement in acute experimental malaria. I. Total hemolytic activity.
Mil Med. 1966 Sep;131(9):Suppl:1173-9.
5
The potential pathogenic role of complement in dengue hemorrhagic shock syndrome.补体在登革出血热休克综合征中的潜在致病作用。
N Engl J Med. 1973 Nov 8;289(19):996-1000. doi: 10.1056/NEJM197311082891902.
6
Biochemical mechanisms of generation of bradykinin by endotoxin.内毒素产生缓激肽的生化机制。
J Infect Dis. 1973 Jul;128:Suppl:144-56. doi: 10.1093/infdis/128.supplement_1.s144.
7
Soluble serum antigens of P. falciparum in nigerians. II. Immunochemical studies.尼日利亚恶性疟原虫的可溶性血清抗原。II. 免疫化学研究。
Afr J Med Sci. 1972 Oct;3(4):309-17.
8
The direct antiglobulin test and immunoconglutinin titres in patients with malaria.
Trans R Soc Trop Med Hyg. 1973;67(1):51-4. doi: 10.1016/0035-9203(73)90319-2.
9
Soluble antigens in the blood of African patients with severe plasmodium falciparum malaria.患有严重恶性疟原虫疟疾的非洲患者血液中的可溶性抗原。
Lancet. 1968 Apr 27;1(7548):881-4. doi: 10.1016/s0140-6736(68)90237-7.
10
Reaction mechanism of the alternative pathway of complement fixation.补体固定替代途径的反应机制。
Lancet. 1973 Mar 3;1(7801):465-7. doi: 10.1016/s0140-6736(73)91886-2.
Zotero 插件