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{Nichols:2015:10.1038/ki.2015.233,
author = {Nichols, EM and Barbour, TD and Pappworth, IY and Wong, EK and Palmer, JM and Sheerin, NS and Pickering, MC and Marchbank, KJ},
doi = {10.1038/ki.2015.233},
journal = {Kidney International},
pages = {1314--1322},
title = {An extended mini-complement factor H molecule ameliorates experimental C3 glomerulopathy.},
url = {http://dx.doi.org/10.1038/ki.2015.233},
volume = {88},
year = {2015}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Abnormal regulation of the complement alternative pathway is associated with C3 glomerulopathy. Complement factor H is the main plasma regulator of the alternative pathway and consists of 20 short consensus repeat (SCR) domains. Although recombinant full-length factor H represents a logical treatment for C3 glomerulopathy, its production has proved challenging. We and others have designed recombinant mini-factor H proteins in which 'non-essential' SCR domains have been removed. Here, we report the in vitro and in vivo effects of a mini-complement factor H protein, FH(1-5^18-20), using the unique factor H-deficient (Cfh-/-) mouse model of C3 glomerulopathy. FH(1-5^18-20) is comprised of the key complement regulatory domains (SCRs 1-5) linked to the surface recognition domains (SCRs 18-20). Intraperitoneal injection of FH(1-5^18-20) in Cfh-/- mice reduced abnormal glomerular C3 deposition, similar to full-length factor H. Systemic effects on plasma alternative pathway control were comparatively modest, in association with a short half-life. Thus, FH(1-5^18-20) is a potential therapeutic agent for C3 glomerulopathy and other renal conditions with alternative pathway-mediated tissue injury.Kidney International advance online publication, 29 July 2015; doi:10.1038/ki.2015.233.
AU  - Nichols,EM
AU  - Barbour,TD
AU  - Pappworth,IY
AU  - Wong,EK
AU  - Palmer,JM
AU  - Sheerin,NS
AU  - Pickering,MC
AU  - Marchbank,KJ
DO  - 10.1038/ki.2015.233
EP  - 1322
PY  - 2015///
SN  - 1523-1755
SP  - 1314
TI  - An extended mini-complement factor H molecule ameliorates experimental C3 glomerulopathy.
T2  - Kidney International
UR  - http://dx.doi.org/10.1038/ki.2015.233
UR  - http://hdl.handle.net/10044/1/26624
VL  - 88
ER  -
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