Imperial College London
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DrCandiceRoufosse

Faculty of Medicine, Department of Immunology and Inflammation

Clinical Reader in Renal Pathology
 
 
 
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Contact

 

+44 (0)20 3313 3280c.roufosse

 
 
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Location

 

Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Turner-Stokes:2020:10.1681/ASN.2019121326,
author = {Turner-Stokes, T and Garcia, Diaz A and Pinheiro, D and Prendecki, M and McAdoo, SP and Roufosse, C and Cook, HT and Pusey, CD and Woollard, KJ},
doi = {10.1681/ASN.2019121326},
journal = {Journal of the American Society of Nephrology},
pages = {1--1},
title = {Live imaging of monocyte subsets in immune complex-mediated glomerulonephritis reveals distinct phenotypes and effector functions.},
url = {http://dx.doi.org/10.1681/ASN.2019121326},
volume = {31},
year = {2020}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - BACKGROUND: Immune complexes within glomerular capillary walls cause crescentic GN (CrGN). Monocytes and macrophages are important in mediating CrGN, but little work has been done to phenotype the subpopulations involved and determine their respective contributions to glomerular inflammation. METHODS: Live glomerular imaging using confocal microscopy monitored intravascular monocyte subset behavior during nephrotoxic nephritis (NTN) in a novel WKY-hCD68-GFP monocyte/macrophage reporter rat strain. Flow cytometry and qPCR further analyzed ex vivo the glomerular leukocyte infiltrate during NTN. RESULTS: Non-classical monocytes surveyed the glomerular endothelium via lymphocyte function-associated antigen 1 (LFA-1) in the steady state. During NTN, non-classical monocytes were recruited first, but subsequent recruitment and retention of classical monocytes was associated with glomerular damage. Monocytes recruited to the glomerular vasculature did not undergo transendothelial migration. This finding suggests that inflammation in immune complex-mediated CrGN is predominantly intravascular, driven by dynamic interactions between intravascular blood monocytes and the endothelium. Glomerular endothelium and non-classical monocytes overexpressed a distinct chemokine axis, which may orchestrate inflammatory myeloid cell recruitment and expression of damage mediators. Reduced classical monocyte recruitment in Lewis rats during NTN confirmed a role for CD16 in mediating glomerular damage. CONCLUSIONS: Monocyte subsets with distinct phenotypes and effector functions may be important in driving inflammation in experimental CrGN resulting from immune complexes formed within the glomerular capillary wall. LFA-1-dependent endothelial surveillance by non-classical monocytes may detect immune complexes through CD16, orchestrating the inflammatory response through intravascular retention of classical monocytes, which results in glomerular damage and proteinuria.
AU  - Turner-Stokes,T
AU  - Garcia,Diaz A
AU  - Pinheiro,D
AU  - Prendecki,M
AU  - McAdoo,SP
AU  - Roufosse,C
AU  - Cook,HT
AU  - Pusey,CD
AU  - Woollard,KJ
DO  - 10.1681/ASN.2019121326
EP  - 1
PY  - 2020///
SN  - 1046-6673
SP  - 1
TI  - Live imaging of monocyte subsets in immune complex-mediated glomerulonephritis reveals distinct phenotypes and effector functions.
T2  - Journal of the American Society of Nephrology
UR  - http://dx.doi.org/10.1681/ASN.2019121326
UR  - https://www.ncbi.nlm.nih.gov/pubmed/32868399
UR  - https://jasn.asnjournals.org/content/early/2020/08/29/ASN.2019121326
UR  - http://hdl.handle.net/10044/1/82578
VL  - 31
ER  -
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