Imperial College London
Alternate

ProfessorMatthewPickering

Faculty of Medicine, Department of Immunology and Inflammation

Centre Director, Professor of Rheumatology
 
 
 
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Contact

 

matthew.pickering Website

 
 
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Assistant

 

Miss Claudia Rocchi +44 (0)20 3313 2315

 
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Location

 

9N12Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Barbour:2016:10.1016/j.kint.2015.11.024,
author = {Barbour, TD and Ling, GS and Ruseva, MM and Fossati-Jimack, L and Cook, HT and Botto, M and Pickering, MC},
doi = {10.1016/j.kint.2015.11.024},
journal = {Kidney International},
pages = {823--832},
title = {Complement receptor 3 mediates renal protection in experimental C3 glomerulopathy},
url = {http://dx.doi.org/10.1016/j.kint.2015.11.024},
volume = {89},
year = {2016}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - C3 glomerulopathy is a complement-mediated renal disease that is frequently associated with abnormalities in regulation of the complement alternative pathway. Mice with deficiency of factor H (Cfh–/–), a negative alternative pathway regulator, are an established experimental model of C3 glomerulopathy in which complement C3 fragments including iC3b accumulate along the glomerular basement membrane. Here we show that deficiency of complement receptor 3 (CR3), the main receptor for iC3b, enhances the severity of spontaneous renal disease in Cfh–/– mice. This effect was found to be dependent on CR3 expression on bone marrow–derived cells. CR3 also mediated renal protection outside the setting of factor H deficiency, as shown by the development of enhanced renal injury in CR3-deficient mice during accelerated nephrotoxic nephritis. The iC3b–CR3 interaction downregulated the proinflammatory cytokine response of both murine and human macrophages to lipopolysaccharide stimulation in vitro, suggesting that the protective effect of CR3 on glomerular injury was mediated via modulation of macrophage-derived proinflammatory cytokines. Thus, CR3 has a protective role in glomerulonephritis and suggests that pharmacologic potentiation of the macrophage CR3 interaction with iC3b could be therapeutically beneficial.
AU  - Barbour,TD
AU  - Ling,GS
AU  - Ruseva,MM
AU  - Fossati-Jimack,L
AU  - Cook,HT
AU  - Botto,M
AU  - Pickering,MC
DO  - 10.1016/j.kint.2015.11.024
EP  - 832
PY  - 2016///
SN  - 1523-1755
SP  - 823
TI  - Complement receptor 3 mediates renal protection in experimental C3 glomerulopathy
T2  - Kidney International
UR  - http://dx.doi.org/10.1016/j.kint.2015.11.024
UR  - http://hdl.handle.net/10044/1/33185
VL  - 89
ER  -
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