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|Title:||Intimal macrophages develop from circulating monocytes during vasculitis.||Austin Authors:||Stock, Angus T;Parsons, Sarah;Sharma, Varun J;James, Fiona L ;Starkey, Graham M ;D'Costa, Rohit;Gordon, Claire L ;Wicks, Ian P||Affiliation:||Department of Medical Biology University of Melbourne Melbourne VIC Australia..
Department of Microbiology and Immunology The Peter Doherty Institute for Infection and Immunity, The University of Melbourne Melbourne VIC Australia..
North Eastern Public Health Unit Austin Health Melbourne VIC Australia..
Rheumatology Unit The Royal Melbourne Hospital Melbourne VIC Australia..
Walter and Eliza Hall Institute of Medical Research Parkville VIC Australia..
Department of Forensic Medicine Monash University Melbourne VIC Australia..
Victorian Institute of Forensic Medicine Melbourne VIC Australia..
Victorian Liver Transplant Unit
Surgery (University of Melbourne)
DonateLife Victoria Carlton VIC Australia..
Department of Intensive Care Medicine Melbourne Health Melbourne VIC Australia..
|Issue Date:||13-Aug-2022||metadata.dc.date:||2022||Publication information:||Clinical & Translational Immunology 2022; 11(8): e1412||Abstract:||Vasculitis is characterised by inflammation of the blood vessels. While all layers of the vessel can be affected, inflammation within the intimal layer can trigger thrombosis and arterial occlusion and is therefore of particular clinical concern. Given this pathological role, we have examined how intimal inflammation develops by exploring which (and how) macrophages come to populate this normally immune-privileged site during vasculitis. We have addressed this question for Kawasaki disease (KD), which is a type of vasculitis in children that typically involves the coronary arteries. We used confocal microscopy and flow cytometry to characterise the macrophages that populate the coronary artery intima in KD patient samples and in a mouse model of KD, and furthermore, have applied an adoptive transfer system to trace how these intimal macrophages develop. In KD patients, intimal hyperplasia coincided with marked macrophage infiltration of the coronary artery intima. Phenotypic analysis revealed that these 'intimal macrophages' did not express markers of resident cardiac macrophages, such as Lyve-1, and instead, were uniformly positive for the chemokine receptor Ccr2, suggesting a monocytic lineage. In support of this origin, we show that circulating monocytes directly invade the intima via transluminal migration during established disease, coinciding with the activation of endothelial cells lining the coronary arteries. During KD, intimal macrophages develop from circulating monocytes that infiltrate the inflamed coronary artery intima by transluminal migration.||URI:||https://ahro.austin.org.au/austinjspui/handle/1/30839||DOI:||10.1002/cti2.1412||ORCID:||https://orcid.org/0000-0002-3386-1857
|Journal:||Clinical & Translational Immunology||PubMed URL:||35991774||PubMed URL:||https://pubmed.ncbi.nlm.nih.gov/35991774/||ISSN:||2050-0068||Type:||Journal Article||Subjects:||Kawasaki disease
|Appears in Collections:||Journal articles|
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