scholarly journals Contribution of Classical Complement Activation and IgM to the Control of Rickettsia Infection

2021 ◽  
Author(s):  
Mustapha Dahmani ◽  
Jack H. Cook ◽  
Jinyi C. Zhu ◽  
Sean P. Riley
Keyword(s):  
Complement Activation ◽  
Classical Complement

scholarly journals Inhibition of classical complement activation attenuates liver ischaemia and reperfusion injury in a rat model

2006 ◽  
Vol 143 (1) ◽  
pp. 15-23 ◽  
Author(s):  
B. H. M. Heijnen ◽  
I. H. Straatsburg ◽  
N. D. Padilla ◽  
G. J. Van Mierlo ◽  
C. E. Hack ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Model ◽  
Complement Activation ◽  
Ischaemia And Reperfusion ◽  
Liver Ischaemia ◽  
Classical Complement

scholarly journals Extracellular Vesicle-Induced Classical Complement Activation Leads to Retinal Endothelial Cell Damage via MAC Deposition

2020 ◽  
Vol 21 (5) ◽  
pp. 1693 ◽  
Author(s):  
Chao Huang ◽  
Kiera P. Fisher ◽  
Sandra S. Hammer ◽  
Julia V. Busik
Keyword(s):  
Extracellular Vesicles ◽  
Complement Activation ◽  
Cell Damage ◽  
Membrane Attack Complex ◽  
Extracellular Vesicle ◽  
Rat Plasma ◽  
Classical Complement Pathway ◽  
Endothelium Damage ◽  
Classical Complement

Several studies have suggested that there is a link between membrane attack complex (MAC) deposition in the retina and the progression of diabetic retinopathy (DR). Our recent investigation demonstrated that circulating IgG-laden extracellular vesicles contribute to an increase in retinal vascular permeability in DR through activation of the complement system. However, the mechanism through which extracellular vesicle-induced complement activation contributes to retinal vascular cytolytic damage in DR is not well understood. In this study, we demonstrate that IgG-laden extracellular vesicles in rat plasma activate the classical complement pathway, and in vitro Streptozotocin (STZ)-induced rat diabetic plasma results in MAC deposition and cytolytic damage in human retinal endothelial cells (HRECs). Moreover, removal of the plasma extracellular vesicles reduced the MAC deposition and abrogated cytolytic damage seen in HRECs. Together, the results of this study demonstrate that complement activation by IgG-laden extracellular vesicles in plasma could lead to MAC deposition and contribute to endothelium damage and progression of DR.

Flow cytometry based detection of HLA alloantibody mediated classical complement activation

2003 ◽  
Vol 275 (1-2) ◽  
pp. 149-160 ◽  
Author(s):  
Markus Wahrmann ◽  
Markus Exner ◽  
Heinz Regele ◽  
Kurt Derfler ◽  
Günther F. Körmöczi ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Complement Activation ◽  
Classical Complement

New insights into the molecular mechanisms of classical complement activation

2010 ◽  
Vol 47 (13) ◽  
pp. 2154-2160 ◽  
Author(s):  
Mihaela Kojouharova ◽  
Kenneth Reid ◽  
Mihaela Gadjeva
Keyword(s):  
Complement Activation ◽  
Molecular Mechanisms ◽  
Classical Complement

scholarly journals Involvement of Antilipoarabinomannan Antibodies in Classical Complement Activation in Tuberculosis

1998 ◽  
Vol 5 (2) ◽  
pp. 211-218 ◽  
Author(s):  
Geir Hetland ◽  
Harald G. Wiker ◽  
Kolbjørn Høgåsen ◽  
Beston Hamasur ◽  
Stefan B. Svenson ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Complement Activation ◽  
Mononuclear Phagocytes ◽  
Factor B ◽  
Tuberculosis Patients ◽  
Terminal Complement Complex ◽  
Classical Activation ◽  
Normal Human ◽  
Terminal Complement ◽  
Classical Complement

ABSTRACT We examined alternative and classical complement activation induced by whole bacilli of Mycobacterium bovis BCG andMycobacterium tuberculosis products. After exposure to BCG, there were higher levels of the terminal complement complex in sera from Indian tuberculosis patients than in sera from healthy controls. The addition of BCG with or without EGTA to these sera indicated that approximately 70 to 85% of the total levels of the terminal complement complex was formed by classical activation. Sera from Indian tuberculosis patients contained more antibody to lipoarabinomannan (LAM) than sera from healthy Indians. Levels of anti-LAM immunoglobulin G2 (IgG2), but not anti-LAM IgM, correlated positively with classical activation induced by BCG in the sera. By flow cytometry, deposition of C3 and terminal complement complex on bacilli incubated with normal human serum was demonstrated. The anticomplement staining was significantly reduced in the presence of EGTA and EDTA. Flow cytometry also revealed the binding of complement to BCG incubated with rabbit anti-LAM and then with factor B-depleted serum. This indicates that classical activation plays a major role in complement activation induced by mycobacteria and that anti-LAM IgG on the bacilli can mediate this response. Classical complement activation may be important for the extent of phagocytosis of M. tuberculosis by mononuclear phagocytes, which may influence the course after infection.

Sign in / Sign up

Export Citation Format

Share Document