ABERRANT PHENOTYPE OF CIRCULATING ANTIGEN PRESENTING CELLS IN GIANT CELL ARTERITIS AND POLYMYLAGIA RHEUMATICA

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Reitsema, R.,1994-Örebro universitet,Institutionen för medicinska vetenskaper,Orebro Univ, Fac Med & Hlth, Orebro, Sweden. (författare)

ABERRANT PHENOTYPE OF CIRCULATING ANTIGEN PRESENTING CELLS IN GIANT CELL ARTERITIS AND POLYMYLAGIA RHEUMATICA

Artikel/kapitelEngelska2023

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HighWire Press,2023
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LIBRIS-ID:oai:DiVA.org:oru-111553
https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-111553URI
https://doi.org/10.1136/annrheumdis-2023-eular.3189DOI

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Språk:engelska
Sammanfattning på:engelska

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Ämneskategori:vet swepub-contenttype
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Background: Giant Cell Arteritis (GCA) and Polymyalgia Rheumatica (PMR) are overlapping diseases occurring exclusively in people older than 50 years. Antigen-presenting cells (APCs), including monocytes and dendritic cells (DCs), are main contributors to the immunopathology of GCA and PMR. In GCA tissues, DCs may be prone to activation, leading to chemokine production and recruitment of CD4+ T-cells and monocytes to the arterial wall. However, little is known about APC phenotypes in the peripheral blood at the time of GCA/PMR diagnosis.Objectives: We aimed to investigate the phenotype of the circulating monocytes and DCs in GCA and PMR patients.Methods: APCs among peripheral blood mononuclear cells (PBMCs) of treatment-naive GCA and PMR patients were compared to those in age- and sex-matched healthy controls (HCs) using flow cytometry (n=15 in each group). Using a 13-colour panel, we identified three monocyte subsets: classical (CD14+CD16-), intermediate (CD14+CD16+), and non-classical (CD14lowCD16+) monocytes. DC subsets were subdivided in CD303+CD11c- plasmacytoid DCs (pDCs), CD11c+CD141+ conventional DCs (cDC1) and CD11c+CD1c+ conventional DCs (cDC2). Each of these subsets was analysed for expression of pattern recognition receptors (Toll-like receptor 4 (TLR4), TLR2) and activation markers (CD86, Programmed Death- Ligand 1 (PD-L1), CD40, HLA-DR, CD11c) by assessing the mean-fluorescence intensity of these markers. Data were analysed by conventional gating strategies and by unsupervised tSNE.Results: GCA and PMR patients displayed a monocytosis, which was due to increases in classical and intermediate monocyte counts, whereas the proportion of non-classical monocytes was reduced. Intermediate monocytes of GCA patients had significantly higher TLR2 expression, a similar trend was observed in non-classical monocytes of GCA and PMR patients. A divergent pattern was observed in the expression of activation markers on classical versus non-classical monocytes: classical monocytes of GCA/PMR patients appeared to be less activated, whereas non-classical monocytes showed an increased marker expression compared to HCs (Figure 1). Even though no differences were observed in DC counts in the peripheral blood, cDC2 counts correlated negatively with CRP levels (r=-0.60 for GCA, r=-0.55 for PMR).Conclusion: Circulating non-classical monocytes, but not DCs, display an activated phenotype in GCA and PMR patients at diagnosis. These cells are thought to be pro-inflammatory, representing the end stage of monocyte maturation in the blood. In contrast, classical monocytes show reduced expression of activation markers in GCA and PMR patients, potentially signalling either an immature or exhausted phenotype. Shown is the mean fluorescence intensity (MFI) of CD11c on the surface of monocyte subsets and CD1c+ conventional dendritic cells (cDC2). Data are shown for patients with giant cell arteritis (GCA) or polymyalgia rheumatica (PMR) and age-matched healthy controls (HCs), n=15 for each group. Statistics by Mann Whitney U. CD11c expression data for pDCs (no CD11c expression) and cDC1 (too small population) are not shown.

Ämnesord och genrebeteckningar

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Reumatologi och inflammation hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Rheumatology and Autoimmunity hsv//eng
Innate immunity
Vasculitis

Biuppslag (personer, institutioner, konferenser, titlar ...)

Hesselink, B. C.University Medical Center Groningen, Rheumatology and Clinical Immunology, Groningen, Netherlands (författare)
Van der Geest, K.University Medical Center Groningen, Rheumatology and Clinical Immunology, Groningen, Netherlands (författare)
Abdulahad, W.University Medical Center Groningen, Rheumatology and Clinical Immunology, Groningen, Netherlands (författare)
Boots, A.University Medical Center Groningen, Rheumatology and Clinical Immunology, Groningen, Netherlands (författare)
Brouwer, E.University Medical Center Groningen, Rheumatology and Clinical Immunology, Groningen, Netherlands (författare)
Heeringa, P.University Medical Center Groningen, Rheumatology and Clinical Immunology, Groningen, Netherlands (författare)
Van Sleen, Y.University Medical Center Groningen, Rheumatology and Clinical Immunology, Groningen, Netherlands (författare)
Örebro universitetInstitutionen för medicinska vetenskaper (creator_code:org_t)

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Ingår i:Annals of the Rheumatic Diseases: HighWire Press82:Suppl. 1, s. 1071-10710003-49671468-2060

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Av författaren/redakt...: Reitsema, R., 19 ...; Hesselink, B. C.; Van der Geest, K ...; Abdulahad, W.; Boots, A.; Brouwer, E.; visa fler...; Heeringa, P.; Van Sleen, Y.; visa färre...

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Av lärosätet: Örebro universitet

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