Literature DB >> 3782799

Recovery of human neutrophils from complement attack: removal of the membrane attack complex by endocytosis and exocytosis.

B P Morgan, J R Dankert, A F Esser.   

Abstract

Nucleated cells can resist lysis by and recover from complement attack even after formation of the potentially cytolytic membrane attack complex on the cell surface. We have found that human neutrophils resist complement lysis by the physical removal of membrane attack complexes by both endocytic and exocytic process. The latter mechanism predominates, vesiculation being detectable within 60 sec of initiating the complement cascade. Sixty-five percent of the formed complexes are removed on plasma membrane vesicles, although only 2% of the cell surface is lost. Ultrastructural examination revealed that these vesicles were covered with ring-like "classical" complement lesions. Analysis of these vesicles by gel electrophoresis indicated that C9 was present exclusively in the form of a sodium dodecyl sulfate-resistant, high m.w. complex. In contrast, the 35% of C9 that remained associated with the cells was found to be inaccessible to a C9-specific monoclonal antibody, and was partly degraded, suggesting internalization of the membrane attack complex and proteolysis of some C9 molecules. The molar ratio of C9 to C8 was 12 to 1 on shed vesicles and on recovered cells.

Entities:  

Mesh:

Substances:

Year:  1987        PMID: 3782799

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  77 in total

1.  Involvement of the ERK mitogen-activated protein kinase in cell resistance to complement-mediated lysis.

Authors:  S Kraus; R Seger; Z Fishelson
Journal:  Clin Exp Immunol       Date:  2001-03       Impact factor: 4.330

2.  CD59 blocks not only the insertion of C9 into MAC but inhibits ion channel formation by homologous C5b-8 as well as C5b-9.

Authors:  Imre Farkas; Lajos Baranyi; Yasushige Ishikawa; Noriko Okada; Csaba Bohata; Denes Budai; Atsuo Fukuda; Masaki Imai; Hidechika Okada
Journal:  J Physiol       Date:  2002-03-01       Impact factor: 5.182

3.  Complement resistance of human carcinoma cells depends on membrane regulatory proteins, protein kinases and sialic acid.

Authors:  N Donin; K Jurianz; L Ziporen; S Schultz; M Kirschfink; Z Fishelson
Journal:  Clin Exp Immunol       Date:  2003-02       Impact factor: 4.330

Review 4.  The role of c5b-9 terminal complement complex in activation of the cell cycle and transcription.

Authors:  Matthew Fosbrink; Florin Niculescu; Horea Rus
Journal:  Immunol Res       Date:  2005       Impact factor: 2.829

5.  Formation of ion-conducting channels by the membrane attack complex proteins of complement.

Authors:  J W Shiver; J R Dankert; A F Esser
Journal:  Biophys J       Date:  1991-10       Impact factor: 4.033

6.  Impaired volume regulation is the mechanism of excitotoxic sensitization to complement.

Authors:  Li Shen Loo; James O McNamara
Journal:  J Neurosci       Date:  2006-10-04       Impact factor: 6.167

7.  Human rheumatoid synovial cell stimulation by the membrane attack complex and other pore-forming toxins in vitro: the role of calcium in cell activation.

Authors:  R H Daniels; B D Williams; B P Morgan
Journal:  Immunology       Date:  1990-11       Impact factor: 7.397

8.  Ectocytosis caused by sublytic autologous complement attack on human neutrophils. The sorting of endogenous plasma-membrane proteins and lipids into shed vesicles.

Authors:  J M Stein; J P Luzio
Journal:  Biochem J       Date:  1991-03-01       Impact factor: 3.857

Review 9.  The role of complement activation in atherosclerosis.

Authors:  Florin Niculescu; Horea Rus
Journal:  Immunol Res       Date:  2004       Impact factor: 2.829

10.  Formation of complement membrane attack complex in mammalian cerebral cortex evokes seizures and neurodegeneration.

Authors:  Zhi-Qi Xiong; Weihua Qian; Katsuaki Suzuki; James O McNamara
Journal:  J Neurosci       Date:  2003-02-01       Impact factor: 6.167

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.