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Articles by Andreas Ramming
CD200 + fibroblasts prime the immunoregulatory function of granulocytic myeloid-derived suppressor cells in inflammatory arthritis
Abstract Granulocytic myeloid-derived suppressor cells (G-MDSCs) are immunoregulatory cells of the neutrophil lineage. Here, we show that immunoregulation by G-MDSCs is imprinted by the joint tissue microenvironment in patients with axial spondyloarthritis and in animal models of inflammatory arthritis. We demonstrate that the suppressive function of G-MDSCs is significantly enhanced in the joint tissue, but not in the circulation.
From psoriatic plaque to synovium: decoding the skin–joint axis in psoriatic arthritis
Abstract Psoriatic arthritis (PsA) develops in up to 30% of individuals with psoriasis, but the mechanisms that drive progression from skin-limited disease to musculoskeletal disease remain incompletely understood. Emerging evidence supports a functional skin–joint axis in which psoriatic plaques function not only as sites of local inflammation but also as sources of immune cells capable of shaping musculoskeletal pathology.
Arthritis susceptibility begins before birth
Why do certain joints develop inflammation in rheumatoid arthritis, while others escape? New findings suggest that the roots of rheumatoid arthritis lie in prenatal tissue architecture.
Deep phenotyping of skin tissue remodeling in patients with systemic sclerosis treated with CD19-CAR T cells
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Abstract Systemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy and fibrotic remodeling of the skin and internal organs. Fibrotic tissue changes are considered hardly reversible with current therapies, suggesting that new strategies are required to modulate the disease-associated molecular and cellular phenotype to enable regeneration of affected tissues.
By Aleix Rius Rigau, Meilin Xu, Ziyuan Liu, Sara Chenguiti Fakhouri, Janina Auth, Panagiotis Garantziotis, Maria Gabriella Raimondo, Carlo Tur, Tim Filla, Markus Eckstein, Fabian Muller, Armin Atzinger, Moritz Ronicke, Arif B. Ekici, Rafael Schmid, Andreas Wirsching, Melanie Hagen, Sebastian Böltz, Tobias Krickau, Raymund E. Horch, Carola Berking, Ricardo Grieshaber-Bouyer, Andreas Ramming, Pooja Gupta, Aline Bozec, Andreas Mackensen, Jörg HW Distler, Georg Schett, Yi-Nan Li, Christina Bergmann, Andrea Zoli, Manoj Kumar Selvaraju, Paula Gehringer
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Nature
Verified
Fibroblast dynamics in colorectal cancer: stability, plasticity, and novel markers
Abstract Colorectal cancer (CRC) is one of the most commonly diagnosed and globally spread malignant diseases. Cancer-associated fibroblasts (CAFs) are key architects of the tumor microenvironment, yet their origin, stability, and interconvertibility remain poorly understood. Using transcriptomic profiling of fibroblasts from colorectal cancer (CRC) patients, we identify highly expressed (HEX) markers that define fibroblast subpopulations and uncover mechanisms governing their plasticity.
GWAS meta-analysis of psoriasis identifies new susceptibility alleles impacting disease mechanisms and therapeutic targets - Nature Communications
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Abstract Psoriasis is a common, debilitating immune-mediated skin disease. Genetic studies have identified biological mechanisms of psoriasis risk, including those targeted by effective therapies. However, the genetic liability to psoriasis is not fully explained by variation at robustly identified risk loci.
By Nick Dand, John Bowes, David Ellinghaus, Jake Saklatvala, Maris Teder-Laving, Laurent Thomas, Allison C. Billi, Matthew Brown Verified, Francesca Capon, Michael Duckworth, Eva Ellinghaus, Oliver FitzGerald, Per Hoffmann, Satveer K. Mahil, Ross McManus, Markus M Nöthen, Jorge R. Oksenberg, Matthew T. Patrick, Andreas Ramming, Jürgen Rech, Mrinal K. Sarkar, Georg Schett, Trilokraj Tejasvi, John Voorhees Verified, Eike Matthias Wacker, Rachael Wasikowski, Stephan Weidinger, Xiaoquan Wen, Anne Barton, Andre Franke, Dafna D Gladman, Johann E. Gudjonsson, Ulrike Hüffmeier, Wilson Liao, Mari Løset, Reedik Mägi, André Reis, Paola Di Meglio, Michael Simpson, Harald Burkhardt
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Nature
Verified
FAPI PET/CT Immune-Fibrosis Imaging for New Insights into Rheumatologic Disorders
Immune-mediated diseases are associated with substantial activation of tissue-resident fibroblasts resulting in fibrosis and organ damage (1). Despite the overall low incidence of fibrotic diseases, fibrotic tissue responses across different diseases have been estimated to account for up to 45% of deaths in high-income countries, causing socioeconomic costs of tens of billions of U.S. dollars per year (2).
FAPI PET/CT Immune-Fibrosis Imaging for New Insights into Rheumatologic Disorders
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Anti-inflammatory and immune-regulatory cytokines in rheumatoid arthritis
Abstract Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by a failure of spontaneous resolution of inflammation. Although the pro-inflammatory cytokines and mediators that trigger RA have been the focus of intense investigations, the regulatory and anti-inflammatory cytokines responsible for the suppression and resolution of disease in a context-dependent manner have been less well characterized.
Inhibition of phosphodiesterase 4 (PDE4) reduces dermal fibrosis by interfering with the release of interleukin-6 from M2 macrophages
Objectives To investigate the disease-modifying effects of phosphodiesterase 4 (PDE4) inhibition in preclinical models of systemic sclerosis (SSc). Methods We studied the effects of PDE4 inhibition in a prevention and a treatment model of bleomycin-induced skin fibrosis, in the topoisomerase mouse model as well as in a model of sclerodermatous chronic graft-versus-host disease.
Elevated serum levels of sonic hedgehog are associated with fibrotic and vascular manifestations in systemic sclerosis
Fibrotic tissue remodelling and vascular alterations cause high morbidity and mortality in patients with systemic sclerosis (SSc).1 2 While the pathogenesis of SSc is only partially understood, recent evidence demonstrates a fundamental role of hedgehog signalling in fibrotic disease manifestations.
Inhibition of phosphodiesterase 4 (PDE4) reduces dermal fibrosis by interfering with the release of interleukin-6 from M2 macrophages
Objectives To investigate the disease-modifying effects of phosphodiesterase 4 (PDE4) inhibition in preclinical models of systemic sclerosis (SSc). Methods We studied the effects of PDE4 inhibition in a prevention and a treatment model of bleomycin-induced skin fibrosis, in the topoisomerase mouse model as well as in a model of sclerodermatous chronic graft-versus-host disease.
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