Rheumatic diseases articles within Nature Communications

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  • Article
    | Open Access

    Antiphospholipid syndrome is characterised by increased neutrophil extracellular trap formation (NETosis) and, consequently, increased thrombotic events. Here Ali et al. show that treatment with adenosine receptor agonists suppresses NETosis and venous thrombosis in mouse models of antiphospholipid syndrome.

    • Ramadan A. Ali
    • , Alex A. Gandhi
    •  & Jason S. Knight

  • Article
    | Open Access

    TMCO1 is a recently described endoplasmic reticular Ca2+ channel. Here, the authors show it is important for osteoblast function and bone formation in mice, and identify a novel pathway linking local increases in Ca2+ at the ER surface with the posttranslational modification of RUNX2.

    • Jianwei Li
    • , Caizhi Liu
    •  & Yingxian Li

  • Article
    | Open Access

    Modulation of the cholinergic pathway and spleen function can reduce inflammation with invasive implants. Here, the authors show that non-invasive ultrasound stimulation of the spleen reduces disease severity in a mouse model of inflammatory arthritis, partly via altering B and T cell function.

    • Daniel P. Zachs
    • , Sarah J. Offutt
    •  & Hubert H. Lim

  • Article
    | Open Access

    Metabolic pathways are increasingly recognized as crucial determinants of T cell function. Here the authors show that the balance between IFNγ and IL-10 production in human CD4 T cells is modulated by the cholesterol biosynthetic pathway.

    • Esperanza Perucha
    • , Rossella Melchiotti
    •  & Andrew P. Cope

  • Article
    | Open Access

    Osteoarthritis is characterised by degeneration of joint cartilage. Here the authors show that the RNA-binding protein ZFP36L1 is upregulated in chondrocytes of humans and mice with osteoarthritis, and that its knockdown in mouse joints protects chondrocytes against apoptosis by modulating the function of heat shock proteins.

    • Young-Ok Son
    • , Hyo-Eun Kim
    •  & Jang-Soo Chun

  • Article
    | Open Access

    The role of innate T cell subsets in the pathogenesis of spondyloarthritis (SpA) is not well understood. Here, the authors examine the role of invariant natural killer T (iNKT) and γδ-T cells in SpA and show that disease-derived iNKT and γδ-T cells have unique and Th17-skewed phenotype and gene expression profiles within inflamed joints.

    • Koen Venken
    • , Peggy Jacques
    •  & Dirk Elewaut

  • Article
    | Open Access

    Cell-free DNA (cfDNA) released from damaged or dead cells can activate DNA sensors that exacerbate the pathogenesis of rheumatoid arthritis (RA). Here the authors use ~40 nm cationic nanoparticles to scavenge cfDNA, and demonstrate the potential for nanomedicine to relieve debilitating RA symptoms.

    • Huiyi Liang
    • , Bo Peng
    •  & Yongming Chen

  • Article
    | Open Access

    Approximately 30% of psoriasis patients develop psoriatic arthritis (PsA) and early diagnosis is crucial for the management of PsA. Here, Patrick et al. develop a computational pipeline involving statistical and machine-learning methods that can assess the risk of progression to PsA based on genetic markers.

    • Matthew T. Patrick
    • , Philip E. Stuart
    •  & Lam C. Tsoi

  • Article
    | Open Access

    Osteoclasts mediate bone disruption in a number of degenerative bone diseases. Here, the authors show that miR-182 regulates osteoclastogenesis via PKR and IFN-beta signaling, is correlated with rheumatoid arthritis, and that its ablation or inhibition is protective against bone erosion in mouse models of osteoporosis or inflammatory arthritis.

    • Kazuki Inoue
    • , Zhonghao Deng
    •  & Baohong Zhao

  • Article
    | Open Access

    Hyperactivation of TGFβ signaling is a common feature of fibrotic diseases. Here the authors show that genetic or pharmacologic inactivation of the tyrosine phosphatase SHP2 prevents TGFβ-induced JAK2/STAT3 signaling, inhibits fibroblast activation and exerts potent anti-fibrotic effects.

    • Ariella Zehender
    • , Jingang Huang
    •  & Jörg H. W. Distler

  • Article
    | Open Access

    Osteocytes reside in a low oxygen environment, but it is not clear if oxygen sensing regulates their function. Here, the authors show that deletion of the oxygen sensor prolyl hydroxylase 2 in osteocytes leads to increased bone mass via regulation of sclerostin, and reduces bone loss in mouse models of osteoporosis.

    • Steve Stegen
    • , Ingrid Stockmans
    •  & Geert Carmeliet

  • Article
    | Open Access

    IFN-γ is central in inflammatory pathogenesis, response to infection and autoimmune diseases. Here the authors show that MMP12 expression is reduced in patients with SLE and that MMP12 post-translationally truncates IFN-y, inhibiting its function and affecting pathogenesis of mouse models of peritonitis, SLE and rheumatoid arthritis.

    • Antoine Dufour
    • , Caroline L. Bellac
    •  & Christopher M. Overall

  • Article
    | Open Access

    Many diseases, such as rheumatoid arthritis, are characterized by a chronic inflammatory state, but it is not clear whether or how this affects the brain. Here, the authors show that the severity of on-going inflammation predicts altered functional brain connectivity in people with rheumatoid arthritis.

    • Andrew Schrepf
    • , Chelsea M. Kaplan
    •  & Neil Basu

  • Article
    | Open Access

    Atherosclerosis and osteoporosis are epidemiologically associated, and oxidation specific epitopes (OSEs), which can be neutralized by innate antibodies, are pathogenic for both. Here, the authors show that mice expressing antibody fragments targeted to OSEs are protected from the bone loss induced by high-fat diet and have increased bone mass when fed a normal diet, and that levels of innate antibodies to OSEs decrease with ageing.

    • Elena Ambrogini
    • , Xuchu Que
    •  & Robert L. Jilka

  • Article
    | Open Access

    Fibroblast-like synoviocytes (FLS) in the intimal layer of the synovium can become invasive and destroy cartilage in patients with rheumatoid arthritis (RA). Here the authors integrate a variety of epigenomic data to map the epigenome of FLS in RA and identify potential therapeutic targets.

    • Rizi Ai
    • , Teresina Laragione
    •  & Gary S. Firestein

  • Article
    | Open Access

    CXCR2 antagonism has been shown to be anti-arthritic, but anti-chemokine therapies usually fail in the clinic owing to redundancy in chemokine-receptor interactions. Here the authors develop single-chain antibodies with multiple chemokine specificities to achieve high affinity and broad specificity to mouse and human CXC chemokines with efficacy in a K/BxN serum transfer model of arthritis.

    • Alessandro Angelini
    • , Yoshishige Miyabe
    •  & K. Dane Wittrup

  • Article
    | Open Access

    Feingold syndrome is a skeletal dysplasia caused by mutations in MYCN or MIR17HG, but it is not clear if these mutations lead to pathology via a common molecular mechanism. Here, the authors show that mutations in MIR17HG lead to upregulated TGF-β signaling in limb mesenchymal cells, while mutations in MYCN downregulate PI3K signaling.

    • Fatemeh Mirzamohammadi
    • , Anastasia Kozlova
    •  & Tatsuya Kobayashi

  • Article
    | Open Access

    The treatment of inflammatory arthritis by local delivery of therapeutics is limited by short half-lives of drugs. Here the authors demonstrate a hydrogel platform that titrates drug release to arthritis activity.

    • Nitin Joshi
    • , Jing Yan
    •  & Jeffrey M. Karp

  • Article
    | Open Access

    Synovial fibroblasts are thought to be central mediators of joint destruction in rheumatoid arthritis (RA). Here the authors use single-cell transcriptomics and flow cytometry to identify synovial fibroblast subsets that are expanded and display distinct tissue distribution and function in patients with RA.

    • Fumitaka Mizoguchi
    • , Kamil Slowikowski
    •  & Michael B. Brenner

  • Article
    | Open Access

    TNF is a major therapeutic target for rheumatoid arthritis (RA) and synovial fibroblasts are central to the pathogenesis of RA. Here the authors dissect TNF-induced death and activation signalling in RA synovial fibroblasts and TNF-driven arthritis and indicate that a successful therapeutic strategy might be to target both IKK2 and RIPK3 at the same time.

    • Marietta Armaka
    • , Caroline Ospelt
    •  & George Kollias

  • Article
    | Open Access

    Osteoclasts are involved in arthritis, and their differentiation depends on RANKL signaling. The author show that the ROS-scavenging protein DJ-1 negatively regulates RANKL signaling and that its ablation increases osteoclast numbers and exacerbates bone damage in mouse models of arthritis.

    • Hyuk Soon Kim
    • , Seung Taek Nam
    •  & Wahn Soo Choi

  • Article
    | Open Access

    STAT3 is a transcription factor that is activated in fibrotic diseases such as systemic sclerosis. Here the authors show that STAT3 is the converging point for multiple pro-fibrotic signalling pathways, and that its genetic ablation or inhibition ameliorate skin fibrosis in mouse models.

    • Debomita Chakraborty
    • , Barbora Šumová
    •  & Jörg H. W. Distler

  • Article
    | Open Access

    Although protein tyrosine kinases are being explored as antifibrotic agents for the treatment of systemic sclerosis, little is known about the function of counteractive protein tyrosine phosphatases in this context. Here, the authors show that PTP4A1 is highly expressed by fibroblasts from patients with systemic sclerosis and promotes TGFβ activity via SRC–ERK–SMAD3 signaling.

    • Cristiano Sacchetti
    • , Yunpeng Bai
    •  & Nunzio Bottini

  • Article
    | Open Access

    Post-translational modifications can affect antibody function in health and disease, but identification of all variants is difficult using existing technologies. Here the authors develop a microfluidic method to identify and quantify low-abundance IgG N-glycans and show some of these IgGs can be used as biomarkers for rheumatoid arthritis.

    • Jing-Rong Wang
    • , Wei-Na Gao
    •  & Zhi-Hong Jiang

  • Article
    | Open Access

    Proliferation of synoviocytes contributes to joint damage in rheumatoid arthritis. Here the authors show that targeting of these cells by a vector, consisting of a baculovirus conjugated to an adenovirus carrying the pro-apoptotic gene PUMA, has therapeutic efficacy in a rat arthritis model.

    • Saw-See Hong
    • , Hubert Marotte
    •  & Pierre Miossec

  • Article
    | Open Access

    DOT1L is one of the few genes linked to osteoarthritis by human GWAS. Here the authors show that DOT1L-dependent histone methylation protects homeostasis of articular chondrocytes by SIRT1-dependent inhibition of canonical WNT signalling, and that inhibition of DOT1L can drive osteoarthritic disease in mice.

    • Silvia Monteagudo
    • , Frederique M. F. Cornelis
    •  & Rik J. Lories

  • Article
    | Open Access

    Osteoarthritis (OA) is a debilitating and destructive joint disease for which disease modifying drugs are not available. Here the authors show that extracellular adenosine signalling via the A2AR receptor on chondrocytes is needed to prevent OA and that liposome-bound adenosine injection can treat the pathology in rats.

    • Carmen Corciulo
    • , Matin Lendhey
    •  & Bruce N. Cronstein

  • Article
    | Open Access

    DEK is a secreted protein abundant in the synovia of patients with juvenile idiopathic arthritis. Here the authors show DEK is important for neutrophil extracellular trap formation and joint inflammation, and demonstrate therapeutic efficacy of DEK-targeting aptamers in a mouse model of arthritis.

    • Nirit Mor-Vaknin
    • , Anjan Saha
    •  & David M. Markovitz

  • Article
    | Open Access

    Rela is a transcription factor shown to have seemingly contradictory roles in anabolism and catabolism of cartilage. Here the authors find that Rela prevents chondrocyte apoptosis and that homozygous knockout causes accelerated osteoarthritis in adults, whereas heterozygous knockout suppresses osteoarthritis by maintaining wild-type effects on apoptosis but inhibiting catabolic gene expression.

    • Hiroshi Kobayashi
    • , Song Ho Chang
    •  & Taku Saito

  • Article
    | Open Access

    MiR-155 is thought to inhibit PU.1 and thereby drive antigen-induced B-cell maturation. Here the authors show that patients with rheumatoid arthritis have high B-cell miR-155 expression and that an antagomir can rescue PU.1 expression, suggesting potential therapeutic avenues to treat rheumatoid arthritis.

    • Stefano Alivernini
    • , Mariola Kurowska-Stolarska
    •  & Gianfranco Ferraccioli

  • Article
    | Open Access

    Osteogenesis imperfecta (OI) is genetically linked to autosomal dominant or autosomal recessive mutations. Here, Marini et al. describe two families with X-chromosome-linked OI with mutations in MBTPS2 that alter regulated intramembrane proteolysis and subsequent defects in collagen crosslinking and osteoblast function.

    • Uschi Lindert
    • , Wayne A. Cabral
    •  & Vorasuk Shotelersuk

  • Article
    | Open Access

    Type 2 immune responses are viewed as opposites of Type 1 and 17 responses. Here the authors show that activation of Type 2 immunity by helminth infection counteracts the development of inflammatory arthritis, a type 17-mediated pathology, via IL-4/IL-13- STAT6 signalling and eosinophil activation.

    • Zhu Chen
    • , Darja Andreev
    •  & Aline Bozec

  • Article
    | Open Access

    Systemic sclerosis (SSc) is a fibrotic disease affecting multiple organs. Here the authors use patient samples plus mouse studies to show a central role for tenascin C as a TLR4 activator responsible for persistence of fibrosis in the context of SSc and SSc-like disease.

    • Swati Bhattacharyya
    • , Wenxia Wang
    •  & John Varga

  • Article
    | Open Access

    Muscle PDGFRβ+ cells are interstitial stem/progenitor cells with myogenic potential. Here, Yao et al. show that PDGFRβ+cell-derived laminin actively regulates their proliferation, differentiation and fate determination.

    • Yao Yao
    • , Erin H. Norris
    •  & Sidney Strickland

  • Article
    | Open Access

    Patients with myotonic dystrophy (MD) suffer from severe cardiac issues of unknown aetiology. Freyermuth et al. show that fatal changes in cardiac electrophysiological properties in humans and mice with MD may arise from misregulation of the alternative splicing of the cardiac Na+ channel SCN5Atranscript, resulting in expression of its fetal form.

    • Fernande Freyermuth
    • , Frédérique Rau
    •  & Nicolas Charlet-Berguerand

  • Article
    | Open Access

    Therapies are needed for the prevention of chondrocyte hypertrophy and thinning of articular cartilage, features of osteoarthritic joint destruction. Here, the authors show that interfering with Sik3 signalling can increase the size of the chondrocyte population and reduce severity of a surgically induced mouse model of osteoarthritis.

    • Yasuhito Yahara
    • , Hiroshi Takemori
    •  & Noriyuki Tsumaki

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