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  1. Article ; Online: Reply.

    Distler, Jörg H W / Hallén, Jonas

    Arthritis & rheumatology (Hoboken, N.J.)

    2024  

    Language English
    Publishing date 2024-02-13
    Publishing country United States
    Document type Letter
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42823
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  2. Article ; Online: Neue molekulare Mechanismen in der Pathophysiologie rheumatologischer Erkrankungen.

    Distler, J H W

    Zeitschrift fur Rheumatologie

    2018  Volume 77, Issue 9, Page(s) 766–768

    Title translation New molecular mechanisms in the pathophysiology of rheumatic diseases.
    MeSH term(s) Autoantibodies ; Humans ; Rheumatic Diseases/immunology ; Rheumatic Diseases/physiopathology
    Chemical Substances Autoantibodies
    Language German
    Publishing date 2018-10-31
    Publishing country Germany
    Document type Editorial
    ZDB-ID 124985-x
    ISSN 1435-1250 ; 0340-1855 ; 0301-6382
    ISSN (online) 1435-1250
    ISSN 0340-1855 ; 0301-6382
    DOI 10.1007/s00393-018-0543-1
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  3. Article ; Online: Reply.

    Soare, Alina / Distler, Jörg H W

    Arthritis & rheumatology (Hoboken, N.J.)

    2020  Volume 73, Issue 1, Page(s) 179–180

    MeSH term(s) Fibroblasts ; Fibrosis ; Humans ; Scleroderma, Systemic
    Language English
    Publishing date 2020-11-17
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.41467
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  4. Article: Response to: 'Correspondence on 'Glucocorticoid-induced relapse of COVID-19 in a patient with sarcoidosis'' by Jeny et al

    Györfi, A. H. / Schett, G. / Distler, J. H. W.

    Ann Rheum Dis

    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #810742
    Database COVID19

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  5. Article ; Online: Apolipoprotein E controls Dectin-1-dependent development of monocyte-derived alveolar macrophages upon pulmonary β-glucan-induced inflammatory adaptation.

    Theobald, H / Bejarano, D A / Katzmarski, N / Haub, J / Schulte-Schrepping, J / Yu, J / Bassler, K / Ament, A L / Osei-Sarpong, C / Piattini, F / Vornholz, L / T'Jonck, W / Györfi, A H / Hayer, H / Yu, X / Sheoran, S / Al Jawazneh, A / Chakarov, S / Haendler, K /
    Brown, G D / Williams, D L / Bosurgi, L / Distler, J H W / Ginhoux, F / Ruland, J / Beyer, M D / Greter, M / Bain, C C / Vazquez-Armendariz, A I / Kopf, M / Schultze, J L / Schlitzer, A

    Nature immunology

    2024  

    Abstract: The lung is constantly exposed to the outside world and optimal adaptation of immune responses is crucial for efficient pathogen clearance. However, mechanisms that lead to lung-associated macrophages' functional and developmental adaptation remain ... ...

    Abstract The lung is constantly exposed to the outside world and optimal adaptation of immune responses is crucial for efficient pathogen clearance. However, mechanisms that lead to lung-associated macrophages' functional and developmental adaptation remain elusive. To reveal such mechanisms, we developed a reductionist model of environmental intranasal β-glucan exposure, allowing for the detailed interrogation of molecular mechanisms of pulmonary macrophage adaptation. Employing single-cell transcriptomics, high-dimensional imaging and flow cytometric characterization paired with in vivo and ex vivo challenge models, we reveal that pulmonary low-grade inflammation results in the development of apolipoprotein E (ApoE)-dependent monocyte-derived alveolar macrophages (ApoE
    Language English
    Publishing date 2024-04-26
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-024-01830-z
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  6. Article ; Online: Mouse Models of Skin Fibrosis.

    Rius Rigau, Aleix / Luber, Markus / Distler, Jörg H W

    Methods in molecular biology (Clifton, N.J.)

    2021  Volume 2299, Page(s) 371–383

    Abstract: Systemic sclerosis (SSc) is a rare systemic autoimmune disease associated with a high mortality. The first histopathological hallmarks are vasculopathy and inflammation, followed by fibrosis of the skin and internal organs. The molecular and cellular ... ...

    Abstract Systemic sclerosis (SSc) is a rare systemic autoimmune disease associated with a high mortality. The first histopathological hallmarks are vasculopathy and inflammation, followed by fibrosis of the skin and internal organs. The molecular and cellular mechanisms are incompletely understood. Rodent models provide important insights into the pathogenesis of SSc and are a mainstay for the development of novel targeted therapies. Here we describe the mechanistic insights of inducible and genetic models, and also discuss in detail the limitations and pitfalls of the most frequently used SSc mouse models. We also describe protocols for running the established bleomycin-induced scleroderma skin fibrosis model.
    MeSH term(s) Animals ; Bleomycin/adverse effects ; Disease Models, Animal ; Fibrosis ; Graft vs Host Disease/genetics ; Graft vs Host Disease/pathology ; Humans ; Mice ; Scleroderma, Systemic/chemically induced ; Scleroderma, Systemic/pathology ; Skin/pathology
    Chemical Substances Bleomycin (11056-06-7)
    Language English
    Publishing date 2021-05-24
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1382-5_25
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  7. Article ; Online: Effect of Anti-S100A4 Monoclonal Antibody Treatment on Experimental Skin Fibrosis and Systemic Sclerosis-Specific Transcriptional Signatures in Human Skin.

    Trinh-Minh, Thuong / Györfi, Andrea-Hermina / Tomcik, Michal / Tran-Manh, Cuong / Zhou, Xiang / Dickel, Nicholas / Tümerdem, Bilgesu Safak / Kreuter, Alexander / Burmann, Sven-Niklas / Borchert, Signe Vedel / Hussain, Rizwan Iqbal / Hallén, Jonas / Klingelhöfer, Jörg / Kunz, Meik / Distler, Jörg H W

    Arthritis & rheumatology (Hoboken, N.J.)

    2024  Volume 76, Issue 5, Page(s) 783–795

    Abstract: Objective: S100A4 is a DAMP protein. S100A4 is overexpressed in patients with systemic sclerosis (SSc), and levels correlate with organ involvement and disease activity. S100A4: Methods: The effects of anti-S100A4 mAbs were evaluated in a bleomycin- ... ...

    Abstract Objective: S100A4 is a DAMP protein. S100A4 is overexpressed in patients with systemic sclerosis (SSc), and levels correlate with organ involvement and disease activity. S100A4
    Methods: The effects of anti-S100A4 mAbs were evaluated in a bleomycin-induced skin fibrosis model and in Tsk-1 mice with a therapeutic dosing regimen. In addition, the effects of anti-S100A4 mAbs on precision cut SSc skin slices were analyzed by RNA sequencing.
    Results: Inhibition of S100A4 was effective in the treatment of pre-established bleomycin-induced skin fibrosis and in regression of pre-established fibrosis with reduced dermal thickening, myofibroblast counts, and collagen accumulation. Transcriptional profiling demonstrated targeting of multiple profibrotic and proinflammatory processes relevant to the pathogenesis of SSc on targeted S100A4 inhibition in a bleomycin-induced skin fibrosis model. Moreover, targeted S100A4 inhibition also modulated inflammation- and fibrosis-relevant gene sets in precision cut SSc skin slices in an ex vivo trial approach. Selected downstream targets of S100A4, such as AMP-activated protein kinase, calsequestrin-1, and phosphorylated STAT3, were validated on the protein level, and STAT3 inhibition was shown to prevent the profibrotic effects of S100A4 on fibroblasts in human skin.
    Conclusion: Inhibition of S100A4 confers dual targeting of inflammatory and fibrotic pathways in complementary mouse models of fibrosis and in SSc skin. These effects support the further development of anti-S100A4 mAbs as disease-modifying targeted therapies for SSc.
    MeSH term(s) Scleroderma, Systemic/drug therapy ; Scleroderma, Systemic/genetics ; Animals ; S100 Calcium-Binding Protein A4/genetics ; S100 Calcium-Binding Protein A4/metabolism ; Humans ; Mice ; Skin/pathology ; Skin/drug effects ; Skin/metabolism ; Fibrosis ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Bleomycin ; Disease Models, Animal ; STAT3 Transcription Factor/metabolism ; Female
    Chemical Substances S100 Calcium-Binding Protein A4 ; Antibodies, Monoclonal ; Bleomycin (11056-06-7) ; STAT3 Transcription Factor ; S100A4 protein, human (142662-27-9)
    Language English
    Publishing date 2024-02-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42781
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  8. Article ; Online: Purinergic signalling in systemic sclerosis.

    Höppner, Jakob / Bruni, Cosimo / Distler, Oliver / Robson, Simon C / Burmester, Gerd R / Siegert, Elise / Distler, Jörg H W

    Rheumatology (Oxford, England)

    2021  Volume 61, Issue 7, Page(s) 2770–2782

    Abstract: SSc is a chronic autoimmune rheumatic disease that involves numerous organs and presents major management challenges. The histopathologic hallmarks of SSc include vasculopathy, fibrosis and autoimmune phenomena involving both innate and adaptive immune ... ...

    Abstract SSc is a chronic autoimmune rheumatic disease that involves numerous organs and presents major management challenges. The histopathologic hallmarks of SSc include vasculopathy, fibrosis and autoimmune phenomena involving both innate and adaptive immune systems. Purinergic signalling is a pathway that may be implicated in the pathophysiology of several of these disease manifestations. Extracellular purines are potent signalling mediators, which have been shown to be dysregulated in SSc. As examples, purines can exacerbate vasculopathy and provoke platelet dysfunction; as well as contributing to immune dysregulation. Elements of purinergic signalling further promote organ and tissue fibrosis in several disease models. Here, we provide an overview of extracellular purine metabolism in purinergic signalling and link disorders of these to the molecular pathology of SSc. We also discuss targeting the purinergic signalling and explore the translational applications for new therapeutic options in SSc.
    MeSH term(s) Fibrosis ; Humans ; Purines/therapeutic use ; Scleroderma, Systemic ; Signal Transduction ; Vascular Diseases
    Chemical Substances Purines
    Language English
    Publishing date 2021-11-27
    Publishing country England
    Document type Journal Article
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/keab859
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  9. Article ; Online: Amelioration of Fibrotic Remodeling of Human 3-Dimensional Full-Thickness Skin by Transglutamase 2 Inhibition.

    Zhou, Xiang / Trinh-Minh, Thuong / Matei, Alexandru-Emil / Györfi, Andrea-Hermina / Hong, Xuezhi / Bergmann, Christina / Schett, Georg / Atkinson, John / Bowcutt, Rowann / Patel, Jessal / Johnson, Timothy S / Distler, Jörg H W

    Arthritis & rheumatology (Hoboken, N.J.)

    2023  Volume 75, Issue 9, Page(s) 1619–1627

    Abstract: Objective: Fibrotic tissues are characterized by excessive crosslinking between extracellular matrix (ECM) proteins, rendering them more resistant to degradation. Although increased crosslinking of ECM is thought to play an important role for ... ...

    Abstract Objective: Fibrotic tissues are characterized by excessive crosslinking between extracellular matrix (ECM) proteins, rendering them more resistant to degradation. Although increased crosslinking of ECM is thought to play an important role for progression of tissue fibrosis, enhanced ECM crosslinking has not yet been targeted therapeutically in systemic sclerosis (SSc). Here, we investigated the role of transglutaminase 2 (TG2), a central crosslinking enzyme, in the activation of SSc fibroblasts.
    Methods: We assessed TG2 expression and activity using TG2 staining, Western blotting, and TG2 activity assays. We inhibited TG2 in fibroblasts cultured under standard 2-dimensional conditions and in a 3-dimensional full-thickness equivalent skin model using monoclonal inhibitory anti-TG2 antibodies.
    Results: TG2 expression was increased in the skin of patients with SSc compared with healthy controls, with levels particularly high in patients with SSc-associated interstitial lung disease. TG2 expression and TG2 activity were also increased in SSc dermal fibroblasts. Moreover, the levels of circulating TG2 in the plasma samples from SSc patients were increased versus samples from healthy controls. Anti-TG2 antibodies did not show consistent antifibrotic effects across different fibroblast cell lines under 2-dimensional culture conditions; however, anti-TG2 antibodies effectively reduced transforming growth factor β-induced dermal thickening, myofibroblast differentiation, and collagen accumulation in the 3-dimensional full-thickness model of human skin.
    Conclusion: We provide the first evidence, to our knowledge, that inhibition of TG2 might be a potential antifibrotic approach in SSc. Our findings have translational potential as anti-TG2 antibodies are currently evaluated in a phase II clinical trial in chronic allograft injury and would thus be available for clinical studies in SSc (ClinicalTrials.gov identifier: NCT04335578).
    MeSH term(s) Humans ; Fibrosis ; Scleroderma, Systemic/pathology ; Collagen/metabolism ; Extracellular Matrix Proteins ; Fibroblasts/metabolism ; Skin/pathology ; Cells, Cultured
    Chemical Substances Collagen (9007-34-5) ; Extracellular Matrix Proteins
    Language English
    Publishing date 2023-07-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42518
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  10. Article ; Online: Identification of a Distinct Monocyte-Driven Signature in Systemic Sclerosis Using Biophysical Phenotyping of Circulating Immune Cells.

    Matei, Alexandru-Emil / Kubánková, Markéta / Xu, Liyan / Györfi, Andrea-Hermina / Boxberger, Evgenia / Soteriou, Despina / Papava, Maria / Prater, Julia / Hong, Xuezhi / Bergmann, Christina / Kräter, Martin / Schett, Georg / Guck, Jochen / Distler, Jörg H W

    Arthritis & rheumatology (Hoboken, N.J.)

    2023  Volume 75, Issue 5, Page(s) 768–781

    Abstract: Objective: Pathologically activated circulating immune cells, including monocytes, play major roles in systemic sclerosis (SSc). Their functional characterization can provide crucial information with direct clinical relevance. However, tools for the ... ...

    Abstract Objective: Pathologically activated circulating immune cells, including monocytes, play major roles in systemic sclerosis (SSc). Their functional characterization can provide crucial information with direct clinical relevance. However, tools for the evaluation of pathologic immune cell activation and, in general, of clinical outcomes in SSc are scarce. Biophysical phenotyping (including characterization of cell mechanics and morphology) provides access to a novel, mostly unexplored layer of information regarding pathophysiologic immune cell activation. We hypothesized that the biophysical phenotyping of circulating immune cells, reflecting their pathologic activation, can be used as a clinical tool for the evaluation and risk stratification of patients with SSc.
    Methods: We performed biophysical phenotyping of circulating immune cells by real-time fluorescence and deformability cytometry (RT-FDC) in 63 SSc patients, 59 rheumatoid arthritis (RA) patients, 28 antineutrophil cytoplasmic antibody-associated vasculitis (AAV) patients, and 22 age- and sex-matched healthy donors.
    Results: We identified a specific signature of biophysical properties of circulating immune cells in SSc patients that was mainly driven by monocytes. Since it is absent in RA and AAV, this signature reflects an SSc-specific monocyte activation rather than general inflammation. The biophysical properties of monocytes indicate current disease activity, the extent of skin or lung fibrosis, and the severity of manifestations of microvascular damage, as well as the risk of disease progression in SSc patients.
    Conclusion: Changes in the biophysical properties of circulating immune cells reflect their pathologic activation in SSc patients and are associated with clinical outcomes. As a high-throughput approach that requires minimal preparations, RT-FDC-based biophysical phenotyping of monocytes can serve as a tool for the evaluation and risk stratification of patients with SSc.
    MeSH term(s) Humans ; Monocytes ; Scleroderma, Systemic/complications ; Pulmonary Fibrosis/pathology ; Skin/pathology ; Arthritis, Rheumatoid
    Language English
    Publishing date 2023-03-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42394
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