Differences in the Complement Activation Induced by Preformed and Nascent Immune Complexes

1991 ◽  
Vol 8 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Tünde Hidvégi ◽  
Lilian Varga ◽  
András Falus ◽  
Michael Kirschfink ◽  
Márta Kókai ◽  
...  
Keyword(s):  
Complement Activation ◽  
Immune Complexes

Cryoglobulins, circulating immune complexes, and complement activation in cerebral malaria.

1981 ◽  
Vol 31 (2) ◽  
pp. 530-535 ◽  
Author(s):  
C Adam ◽  
M Géniteau ◽  
M Gougerot-Pocidalo ◽  
P Verroust ◽  
J Lebras ◽  
...  
Keyword(s):  
Cerebral Malaria ◽  
Complement Activation ◽  
Immune Complexes ◽  
Circulating Immune Complexes

Breakdown of C3 Covalently Bound to F(ab')(2) Immune Complexes after Complement Activation by the Alternative Pathway

Complement ◽  
1986 ◽  
Vol 3 (2) ◽  
pp. 53-62 ◽  
Author(s):  
L.C. Antón ◽  
J.M. Alcolea ◽  
G. Marqués ◽  
P. Sánchez-Corral ◽  
F. Vivanco
Keyword(s):  
Complement Activation ◽  
Immune Complexes ◽  
Alternative Pathway ◽  
Covalently Bound

Collectin11 and Complement Activation in IgA Nephropathy

2021 ◽  
pp. CJN.04300321
Author(s):  
Min Wei ◽  
Wei-yi Guo ◽  
Bo-yang Xu ◽  
Su-fang Shi ◽  
Li-jun Liu ◽  
...  
Keyword(s):  
Iga Nephropathy ◽  
Complement Activation ◽  
Immune Complexes ◽  
Mesangial Cells ◽  
Kidney Injury ◽  
Lectin Pathway ◽  
Independent Manner ◽  
Proximity Ligation ◽  
Injury Model

Background and objectives: IgA nephropathy is the most common primary glomerulonephritis worldwide. Previous research demonstrated that collectin11, an initiator of complement lectin pathway, was involved in both acute kidney injury and chronic tubulointerstitial fibrosis. Here, we investigated the potential role of collectin11 in the pathogenesis of IgA nephropathy. Design, setting, participants, and measurements: The deposition of collectin11 and other complement proteins was detected in glomeruli of 60 participants with IgA nephropathy by immunofluorescence. In vitro, human mesangial cells were treated with IgA1-containing immune complexes derived from participants with IgA nephropathy. Then, the expression of collectin11 in mesangial cells was examined by RT-qPCR and immunofluorescence. The codeposition of collctin11 with IgA1 or C3 on mesangial cells was detected by immunofluorescence and proximity ligation assays. Results: 37% participants with IgA nephropathy (22/60) showed codeposition of collectin11 with IgA in the glomerular mesangium. Using an injury model of mesangial cells, we demonstrated that IgA1-immune complexes derived from participants with IgA nephropathy increased the secretion of collectin11 in mesangial cells with the subsequent deposition of collectin11 on the cell surface via the interaction with deposited IgA1-immune complexes. In vitro, we found that collectin11 bound to IgA1-immune complexes in a dose-dependent but calcium-independent manner. Furthermore, deposited collectin11 initiated the activation of complement and accelerated the deposition of C3 on mesangial cells. Conclusions: In situ-produced collectin11 by mesangial cells might play an essential role in kidney injury in a subset of patients with IgA nephropathy through the induction of complement activation.

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