Imperial College London

DrJamesPease

Faculty of MedicineNational Heart & Lung Institute

Reader in Leukocyte Biology
 
 
 
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Contact

 

+44 (0)20 7594 3162j.pease Website

 
 
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Location

 

109Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Weiss:2015:10.1073/pnas.1506254112,
author = {Weiss, M and Byrne, AJ and Blazek, K and Saliba, DG and Pease, JE and Perocheau, D and Feldmann, M and Udalova, IA},
doi = {10.1073/pnas.1506254112},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
pages = {11001--11006},
title = {IRF5 controls both acute and chronic inflammation},
url = {http://dx.doi.org/10.1073/pnas.1506254112},
volume = {112},
year = {2015}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Whereas the importance of macrophages in chronic inflammatory diseases is well recognized, there is an increasing awareness that neutrophils may also play an important role. In addition to the well-documented heterogeneity of macrophage phenotypes and functions, neutrophils also show remarkable phenotypic diversity among tissues. Understanding the molecular pathways that control this heterogeneity should provide abundant scope for the generation of more specific and effective therapeutics. We have shown that the transcription factor IFN regulatory factor 5 (IRF5) polarizes macrophages toward an inflammatory phenotype. IRF5 is also expressed in other myeloid cells, including neutrophils, where it was linked to neutrophil function. In this study we explored the role of IRF5 in models of acute inflammation, including antigen-induced inflammatory arthritis and lung injury, both involving an extensive influx of neutrophils. Mice lacking IRF5 accumulate far fewer neutrophils at the site of inflammation due to the reduced levels of chemokines important for neutrophil recruitment, such as the chemokine (C-X-C motif) ligand 1. Furthermore we found that neutrophils express little IRF5 in the joints and that their migratory properties are not affected by the IRF5 deficiency. These studies extend prior ones suggesting that inhibiting IRF5 might be useful for chronic macrophage-induced inflammation and suggest that IRF5 blockade would ameliorate more acute forms of inflammation, including lung injury.
AU - Weiss,M
AU - Byrne,AJ
AU - Blazek,K
AU - Saliba,DG
AU - Pease,JE
AU - Perocheau,D
AU - Feldmann,M
AU - Udalova,IA
DO - 10.1073/pnas.1506254112
EP - 11006
PY - 2015///
SN - 0027-8424
SP - 11001
TI - IRF5 controls both acute and chronic inflammation
T2 - Proceedings of the National Academy of Sciences of the United States of America
UR - http://dx.doi.org/10.1073/pnas.1506254112
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000360383200058&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - https://www.pnas.org/content/112/35/11001/
VL - 112
ER -