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CD163 and CD206 expression define distinct macrophage subsets involved in active ANCA-associated glomerulonephritis

Aendekerk, Joop P. ; Jiemy, William F. ; Raveling-Eelsing, Elisabeth ; [et al.]

Elsevier BV ; 2022

In: Journal of Autoimmunity Vol. 133 ( 2022-12), p. 102914-

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In: Journal of Autoimmunity, Elsevier BV, Vol. 133 ( 2022-12), p. 102914-

Type of Medium: Online Resource

ISSN: 0896-8411

URL: Article

DOI: 10.1016/j.jaut.2022.102914

RVK:

XA 52099

Language: English

Publisher: Elsevier BV

Publication Date: 2022

detail.hit.zdb_id: 1468989-3

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Giant worm-shaped ESCRT scaffolds surround actin-independent integrin clusters

Stempels, Femmy C. ; Jiang, Muwei ; Warner, Harry M. ; [et al.]

Rockefeller University Press ; 2023

In: Journal of Cell Biology Vol. 222, No. 7 ( 2023-07-03)

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In: Journal of Cell Biology, Rockefeller University Press, Vol. 222, No. 7 ( 2023-07-03)

Abstract: Endosomal Sorting Complex Required for Transport (ESCRT) proteins can be transiently recruited to the plasma membrane for membrane repair and formation of extracellular vesicles. Here, we discovered micrometer-sized worm-shaped ESCRT structures that stably persist for multiple hours at the plasma membrane of macrophages, dendritic cells, and fibroblasts. These structures surround clusters of integrins and known cargoes of extracellular vesicles. The ESCRT structures are tightly connected to the cellular support and are left behind by the cells together with surrounding patches of membrane. The phospholipid composition is altered at the position of the ESCRT structures, and the actin cytoskeleton is locally degraded, which are hallmarks of membrane damage and extracellular vesicle formation. Disruption of actin polymerization increased the formation of the ESCRT structures and cell adhesion. The ESCRT structures were also present at plasma membrane contact sites with membrane-disrupting silica crystals. We propose that the ESCRT proteins are recruited to adhesion-induced membrane tears to induce extracellular shedding of the damaged membrane.

Type of Medium: Online Resource

ISSN: 0021-9525 , 1540-8140

URL: Article

DOI: 10.1083/jcb.202205130

RVK:

WA 15000

Language: English

Publisher: Rockefeller University Press

Publication Date: 2023

detail.hit.zdb_id: 1421310-2

SSG: 12

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Novel PET Imaging of Inflammatory Targets and Cells for the Diagnosis and Monitoring of Giant Cell Arteritis and Polymyalgia Rheumatica

van der Geest, Kornelis S. M. ; Sandovici, Maria ; Nienhuis, Pieter H. ; [et al.]

Frontiers Media SA ; 2022

In: Frontiers in Medicine Vol. 9 ( 2022-6-6)

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In: Frontiers in Medicine, Frontiers Media SA, Vol. 9 ( 2022-6-6)

Abstract: Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are two interrelated inflammatory diseases affecting patients above 50 years of age. Patients with GCA suffer from granulomatous inflammation of medium- to large-sized arteries. This inflammation can lead to severe ischemic complications (e.g., irreversible vision loss and stroke) and aneurysm-related complications (such as aortic dissection). On the other hand, patients suffering from PMR present with proximal stiffness and pain due to inflammation of the shoulder and pelvic girdles. PMR is observed in 40–60% of patients with GCA, while up to 21% of patients suffering from PMR are also affected by GCA. Due to the risk of ischemic complications, GCA has to be promptly treated upon clinical suspicion. The treatment of both GCA and PMR still heavily relies on glucocorticoids (GCs), although novel targeted therapies are emerging. Imaging has a central position in the diagnosis of GCA and PMR. While [ 18 F]fluorodeoxyglucose (FDG)-positron emission tomography (PET) has proven to be a valuable tool for diagnosis of GCA and PMR, it possesses major drawbacks such as unspecific uptake in cells with high glucose metabolism, high background activity in several non-target organs and a decrease of diagnostic accuracy already after a short course of GC treatment. In recent years, our understanding of the immunopathogenesis of GCA and, to some extent, PMR has advanced. In this review, we summarize the current knowledge on the cellular heterogeneity in the immunopathology of GCA/PMR and discuss how recent advances in specific tissue infiltrating leukocyte and stromal cell profiles may be exploited as a source of novel targets for imaging. Finally, we discuss prospective novel PET radiotracers that may be useful for the diagnosis and treatment monitoring in GCA and PMR.

Type of Medium: Online Resource

ISSN: 2296-858X

URL: Article

DOI: 10.3389/fmed.2022.902155

Language: Unknown

Publisher: Frontiers Media SA

Publication Date: 2022

detail.hit.zdb_id: 2775999-4

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Table_1.docx

van Nieuwland, Marieke ; Esen, Idil ; Reitsema, Rosanne D. ; [et al.]

Frontiers Media SA ; 2023

In: Frontiers in Immunology Vol. 14 ( 2023-6-16)

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In: Frontiers in Immunology, Frontiers Media SA, Vol. 14 ( 2023-6-16)

Abstract: Giant cell arteritis (GCA) is a vasculitis of the medium- and large-sized arteries. Interferon type I (IFN-I) is increasingly recognized as a key player in autoimmune diseases and might be involved in GCA pathogenesis, however evidence is limited. IFN-I activates Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathways, leading to increased expression of interferon stimulated genes. In this study, IFN-I activity in GCA is explored, focusing on CD8+ T cells. Methods Expression of phospho-STAT (pSTAT) 1, 3 and 5 was investigated in IFN-α-stimulated peripheral mononuclear cells (PBMCs) gated separately for CD8+ T cells of patients with GCA (n=18), healthy controls (HC, n=15) and infection controls (n=11) by Phosphoflow method combined with fluorescent cell barcoding technique. Furthermore, IFN-I induced myxovirus-resistance protein A (MxA) and CD8+ T cell expression was investigated by immunohistochemistry in temporal artery biopsies (TAB) of GCA patients (n=20) and mimics (n=20), and in aorta tissue of GCA (n=8) and atherosclerosis patients (n=14). Results pSTAT1 expression was increased in IFN-α stimulated CD8+ T cells from GCA patients, whereas no difference was observed in pSTAT3 and pSTAT5 expression. MxA was present in TABs of 13/20 GCA patients compared to 2/20 mimics and in 8/8 GCA+ compared to 13/14 GCA- aorta tissues. MxA location partially co-localized with CD8+T cells. Conclusions Our results provide evidence for increased IFN-I activity in CD8+ T cells of GCA patients, both systemically and locally. These findings warrant further investigation regarding IFN-I induced biomarkers and IFN-I related novel therapeutic options in GCA.

Type of Medium: Online Resource

ISSN: 1664-3224

URL: Article

DOI: 10.3389/fimmu.2023.1197293

DOI: 10.3389/fimmu.2023.1197293.s001

DOI: 10.3389/fimmu.2023.1197293.s002

DOI: 10.3389/fimmu.2023.1197293.s003

DOI: 10.3389/fimmu.2023.1197293.s004

Language: Unknown

Publisher: Frontiers Media SA

Publication Date: 2023

detail.hit.zdb_id: 2606827-8

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Altered Plasma Levels and Tissue Expression of Fibroblast Activation Protein Alpha in Giant Cell Arteritis

Xu, Shuang ; Jiemy, William F. ; Boots, Annemieke M. H. ; [et al.]

Wiley ; 2024

In: Arthritis Care & Research Vol. 76, No. 9 ( 2024-09), p. 1322-1332

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In: Arthritis Care & Research, Wiley, Vol. 76, No. 9 ( 2024-09), p. 1322-1332

Abstract: Giant cell arteritis (GCA) is characterized by granulomatous inflammation of the medium‐ and large‐sized arteries accompanied by remodeling of the vessel wall. Fibroblast activation protein alpha (FAP) is a serine protease that promotes both inflammation and fibrosis. Here, we investigated the plasma levels and vascular expression of FAP in GCA. Methods Plasma FAP levels were measured with enzyme‐linked immunosorbent assay in treatment‐naive patients with GCA (n = 60) and polymyalgia rheumatica (PMR) (n = 63) compared with age‐ and sex‐matched healthy controls (HCs) (n = 42) and during follow‐up, including treatment‐free remission (TFR). Inflamed temporal artery biopsies (TABs) of patients with GCA (n = 9), noninflamed TABs (n = 14), and aorta samples from GCA‐related (n = 9) and atherosclerosis‐related aneurysm (n = 11) were stained for FAP using immunohistochemistry. Immunofluorescence staining was performed for fibroblasts (CD90), macrophages (CD68/CD206/folate receptor beta), vascular smooth muscle cells (desmin), myofibroblasts (α‐smooth muscle actin), interleukin‐6 (IL‐6), and matrix metalloproteinase‐9 (MMP‐9). Results Baseline plasma FAP levels were significantly lower in patients with GCA compared with patients with PMR and HCs and inversely correlated with systemic markers of inflammation and angiogenesis. FAP levels decreased even further at 3 months on remission in patients with GCA and gradually increased to the level of HCs in TFR. FAP expression was increased in inflamed TABs and aorta of patients with GCA compared with control tissues. FAP was abundantly expressed in fibroblasts and macrophages. Some of the FAP + fibroblasts expressed IL‐6 and MMP‐9. Conclusion FAP expression in GCA is clearly modulated both in plasma and in vessels. FAP may be involved in the inflammatory and remodeling processes in GCA and have utility as a target for imaging and therapeutic intervention.

Type of Medium: Online Resource

ISSN: 2151-464X , 2151-4658

URL: Issue

URL: Article

DOI: 10.1002/acr.v76.9

DOI: 10.1002/acr.25354

RVK:

XA 30325

Language: English

Publisher: Wiley

Publication Date: 2024

detail.hit.zdb_id: 2016713-1

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Comment on: Plasma Pyruvate Kinase M2 as a marker of vascular inflammation in giant cell arteritis: reply

Esen, Idil ; Jiemy, William F ; van Sleen, Yannick ; [et al.]

Oxford University Press (OUP) ; 2022

In: Rheumatology Vol. 61, No. 7 ( 2022-07-06), p. e185-e187

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In: Rheumatology, Oxford University Press (OUP), Vol. 61, No. 7 ( 2022-07-06), p. e185-e187

Type of Medium: Online Resource

ISSN: 1462-0324 , 1462-0332

URL: Article

DOI: 10.1093/rheumatology/keac093

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2022

detail.hit.zdb_id: 1474143-X

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Phenotypic, transcriptomic and functional profiling reveal reduced activation thresholds of CD8+ T cells in giant cell arteritis

Reitsema, Rosanne D ; van der Geest, Kornelis S M ; Sandovici, Maria ; [et al.]

Oxford University Press (OUP) ; 2022

In: Rheumatology Vol. 62, No. 1 ( 2022-12-23), p. 417-427

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In: Rheumatology, Oxford University Press (OUP), Vol. 62, No. 1 ( 2022-12-23), p. 417-427

Abstract: Evidence from temporal artery tissue and blood suggests involvement of CD8+ T cells in the pathogenesis of GCA, but their exact role is poorly understood. Therefore, we performed a comprehensive analysis of circulating and lesional CD8+ T cells in GCA patients. Methods Circulating CD8+ T cells were analysed for differentiation status (CD45RO, CCR7), markers of activation (CD69 and CD25) and proliferation (Ki-67) in 14 newly diagnosed GCA patients and 18 healthy controls by flow cytometry. Proliferative capacity of CD8+ T cells upon anti-CD3 and anti-CD3/28 in vitro stimulation was assessed. Single-cell RNA sequencing of peripheral blood mononuclear cells of patients and controls (n = 3 each) was performed for mechanistic insight. Immunohistochemistry was used to detect CD3, CD8, Ki-67, TNF-α and IFN-γ in GCA-affected tissues. Results GCA patients had decreased numbers of circulating effector memory CD8+ T cells but the percentage of Ki-67-expressing effector memory CD8+ T cells was increased. Circulating CD8+ T cells from GCA patients demonstrated reduced T cell receptor activation thresholds and displayed a gene expression profile that is concurrent with increased proliferation. CD8+ T cells were detected in GCA temporal arteries and aorta. These vascular CD8+ T cells expressed IFN-γ but not Ki-67. Conclusion In GCA, circulating effector memory CD8+ T cells demonstrate a proliferation-prone phenotype. The presence of CD8+ T cells in inflamed arteries seems to reflect recruitment of circulating cells rather than local expansion. CD8+ T cells in inflamed tissues produce IFN-γ, which is an important mediator of local inflammatory responses in GCA.

Type of Medium: Online Resource

ISSN: 1462-0324 , 1462-0332

URL: Article

DOI: 10.1093/rheumatology/keac250

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2022

detail.hit.zdb_id: 1474143-X

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The immune pathology of bursitis in rheumatic inflammatory diseases, degenerative conditions and mechanical stress: A systematic review

Zhang, Anqi ; Brouwer, Elisabeth ; Sandovici, Maria ; [et al.]

Elsevier BV ; 2024

In: Seminars in Arthritis and Rheumatism Vol. 68 ( 2024-10), p. 152527-

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In: Seminars in Arthritis and Rheumatism, Elsevier BV, Vol. 68 ( 2024-10), p. 152527-

Type of Medium: Online Resource

ISSN: 0049-0172

URL: Article

DOI: 10.1016/j.semarthrit.2024.152527

Language: English

Publisher: Elsevier BV

Publication Date: 2024

detail.hit.zdb_id: 2048942-0

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Expression of interleukin-6 in synovial tissue of patients with polymyalgia rheumatica

Jiemy, William F ; Zhang, Anqi ; Boots, Annemieke M H ; [et al.]

BMJ ; 2023

In: Annals of the Rheumatic Diseases Vol. 82, No. 3 ( 2023-03), p. 1-2

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In: Annals of the Rheumatic Diseases, BMJ, Vol. 82, No. 3 ( 2023-03), p. 1-2

Type of Medium: Online Resource

ISSN: 0003-4967 , 1468-2060

URL: Article

DOI: 10.1136/ard-2022-222873

RVK:

XA 10000

Language: English

Publisher: BMJ

Publication Date: 2023

detail.hit.zdb_id: 1481557-6

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Distinct macrophage phenotypes skewed by local granulocyte macrophage colony‐stimulating factor (GM‐CSF) and macrophage colony‐stimulating factor (M‐CSF) are associated with tissue destruction and intimal hyperplasia in giant cell arteritis

Jiemy, William F ; van Sleen, Yannick ; van der Geest, Kornelis SM ; [et al.]

Wiley ; 2020

In: Clinical & Translational Immunology Vol. 9, No. 9 ( 2020-01)

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In: Clinical & Translational Immunology, Wiley, Vol. 9, No. 9 ( 2020-01)

Abstract: To determine the presence and spatial distribution of different macrophage phenotypes, governed by granulocyte macrophage colony‐stimulating factor (GM‐CSF) and macrophage colony‐stimulating factor (M‐CSF) skewing signals, in giant cell arteritis (GCA) lesions. Methods Temporal artery biopsies (TABs, n = 11) from treatment‐naive GCA patients, aorta samples from GCA‐related aneurysms ( n = 10) and atherosclerosis ( n = 10) were stained by immunohistochemistry targeting selected macrophage phenotypic markers, cytokines, matrix metalloproteinases (MMPs) and growth factors. In vitro macrophage differentiation ( n = 10) followed by flow cytometry, Luminex assay and ELISA were performed to assess whether GM‐CSF and M‐CSF are drivers of macrophage phenotypic heterogeneity. Results A distinct spatial distribution pattern of macrophage phenotypes in TABs was identified. CD206 + /MMP‐9 + macrophages were located at the site of tissue destruction, whereas FRβ + macrophages were located in the inner intima of arteries with high degrees of intimal hyperplasia. Notably, this pattern was also observed in macrophage‐rich areas in GCA aortas but not in atherosclerotic aortas. Flow cytometry showed that GM‐CSF treatment highly upregulated CD206 expression, while FRβ was expressed by M‐CSF‐skewed macrophages, only. Furthermore, localised expression of GM‐CSF and M‐CSF was detected, likely contributing to macrophage heterogeneity in the vascular wall. Conclusions Our data document a distinct spatial distribution pattern of CD206 + /MMP‐9 + macrophages and FRβ + macrophages in GCA linked to tissue destruction and intimal proliferation, respectively. We suggest that these distinct macrophage phenotypes are skewed by sequential GM‐CSF and M‐CSF signals. Our study adds to a better understanding of the development and functional role of macrophage phenotypes in the pathogenesis of GCA and opens opportunities for the design of macrophage‐targeted therapies.

Type of Medium: Online Resource

ISSN: 2050-0068 , 2050-0068

URL: Issue

URL: Article

DOI: 10.1002/cti2.v9.9

DOI: 10.1002/cti2.1164

Language: English

Publisher: Wiley

Publication Date: 2020

detail.hit.zdb_id: 2694482-0

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