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Regulation of peripheral classical and non-classical monocytes on infliximab treatment in patients with rheumatoid arthritis and ankylosing spondylitis

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author daniel aeberli richrd k. kamgang deepak balani willy hofstetter peter m. villiger michael seitz,
Project Osteoklastogenese und chronisch entzündliche rheumatische Erkrankungen
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Original article (peer-reviewed)

Journal RMD Open
Volume (Issue) 2016; 2(e000079)
Page(s) 1 - 5
Title of proceedings RMD Open
DOI 10.1136/rmdopen-2015-000079

Open Access

URL http://dx.doi.org/10.1136/rmdopen-2015-000079
Type of Open Access Publisher (Gold Open Access)

Abstract

Objective: To investigate the regulatory effect of tumour necrosis factor (TNF) blockade with infliximab on the distribution of peripheral blood monocyte subpopulations in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Methods: Purified CD11b+CD14+ monocytes from 5 patients with RA and 5 AS were analysed ex vivo before and after infliximab treatment by flow cytometry for CD16, CD163, CD11b, C-C chemokine receptor type 2 (CCR2) and CXC chemokine receptor 4 (CXCR4) at baseline and at days 2, 14, 84 and 168 after the first infliximab administration. Serum levels of the stromal cell-derived factor (SDF)-1 and monocyte chemotactic peptide (MCP)-1 at different time points were measured in either patient group before and on infliximab treatment. Results: Anti-TNF treatment with infliximab led to a significant increase of circulating CD11b+ non-classical and a concomitantly decrease of CD11b+ classical monocytes, to a decline in SDF-1 levels and reduced expression of CCR2 and CXCR4 on non-classical monocyte subpopulation. Conclusions: Our study shows, that TNFα blockade by infliximab resulted in a dichotomy of the regulation of classical and non-classical monocytes that might have substantial impact on inhibition of osteoclastogenesis and of subsequent juxta-articular bone destruction and systemic bone loss in RA
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