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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Expression of DARC, CXCR3 and CCR5 in giant cell arteritis
H Brühl1, V Vielhauer, M Weiss
1Medical Policlinic, University of Munich, Munich, Germany. hilke.bruehl@med.uni-muenchen.de
Insights
Giant cell arteritis (GCA) involves significant leucocyte infiltration, driven by chemokines. This study found key chemokine receptors (CCR5, CXCR3) and DARC are highly expressed in GCA lesions, suggesting their role in leucocyte migration.
Area of Science:
- Immunology
- Pathology
- Rheumatology
Background:
- Leucocyte infiltration is central to vasculitis, with chemokines mediating this process.
- Giant cell arteritis (GCA) is an inflammatory condition affecting arteries.
Purpose of the Study:
- To compare the local expression of chemokines and chemokine receptors in GCA biopsies versus polymyalgia rheumatica (PMR) arteries.
- To investigate the expression of CCR5, CXCR3, Duffy antigen/receptor of chemokine (DARC), and RANTES/CCL5 in GCA.
Main Methods:
- Immunohistological analysis of paraffin-embedded tissue sections from GCA and PMR patients.
- In situ hybridization to detect RANTES/CCL5 mRNA in tissue sections.
Main Results:
- High expression of CCR5 and CXCR3 on infiltrating leucocytes in GCA tissue.
- Co-localization of CCR5+, CXCR3+ leucocytes with CCL5/RANTES mRNA in the adventitia of GCA arteries.
- Marked DARC expression on adventitial high endothelial venules in GCA, contrasting with low expression in PMR.
Conclusions:
- The findings suggest a role for CCR5, CXCR3, and DARC in leucocyte infiltration in GCA.
- DARC may support leucocyte infiltration by mediating vascular presentation of chemokines in vasculitis lesions.
Objectives:
Leucocyte infiltration is the hallmark of vasculitis, chemokines being mainly responsible for leucocyte migration into inflamed tissues. The objective was to evaluate the local expression of chemokines and chemokine receptors in biopsies of patients with giant cell arteritis (GCA) compared with arteries from patients with polymyalgia rheumatica (PMR). We studied the expression of CCR5, CXCR3 and that of the Duffy antigen/receptor of chemokine (DARC), a chemokine internalizing receptor (interceptor), in parallel to the expression of the CCR5 ligand RANTES/CCL5.
Methods:
Paraffin-embedded tissue sections from six patients with GCA and five patients with PMR were available for immunohistological analysis of chemokine receptor expression. RANTES/CCL5 mRNA was detected in tissue sections by in situ hybridization.
Results:
In patients with biopsy-proven giant cell arteritis, CCR5 and CXCR3 were highly expressed by infiltrating leucocytes in involved tissue sections. Predominant clustering of CCR5+ and CXCR3+ leucocytes was found in the adventitia and was co-localized with the expression of CCL5/RANTES mRNA. Interestingly, we found marked expression of DARC on adventitial high endothelial venules in vasculitis lesions of patients with GCA, while in arteries from patients with PMR DARC was only expressed on a low number of vessels with flat lining endothelium.
Conclusions:
The co-localization of infiltrating CCR5+ and CXCR3+ leucocytes together with CCL5/RANTES and DARC in vasculitis lesions suggests a role for these chemokine receptors in leucocyte infiltration, possibly supported by DARC-mediated vascular presentation of chemokines.
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