Rheumatoid arthritis articles within Nature Communications

Featured

• Article
  21 June 2017 | Open Access

  Somatic mutations in clonally expanded cytotoxic T lymphocytes in patients with newly diagnosed rheumatoid arthritis

  Accumulation of somatic mutations in lymphocytes is a feature of some cancers. Here the authors show that patients with recent onset of rheumatoid arthritis also accumulate mutations in their expanded CD8+ effector memory T cell pool independent of cancer association.

  • P. Savola
  • , T. Kelkka
  •  & S. Mustjoki

• Article
  23 March 2017 | Open Access

  Epigenetically-driven anatomical diversity of synovial fibroblasts guides joint-specific fibroblast functions

  Arthritis affects different joints variably despite systemic inflammatory cues. Here the authors show anatomical differences in the transcriptome, epigenome and function of synovial fibroblasts that might affect susceptibility to site-specific joint diseases.

  • Mojca Frank-Bertoncelj
  • , Michelle Trenkmann
  •  & Caroline Ospelt

• Article
  27 September 2016 | Open Access

  MicroRNA-155 influences B-cell function through PU.1 in rheumatoid arthritis

  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
  10 June 2016 | Open Access

  Joint-specific DNA methylation and transcriptome signatures in rheumatoid arthritis identify distinct pathogenic processes

  Rheumatoid arthritis is an inflammatory disease that selectively affects different joints. Here the authors show that gene expression and DNA methylation patterns of fibroblast-like synoviocytes differ between hip and knee joints in patients with RA, thus providing epigenetic and transcriptomic evidence for this anatomic selectivity of inflammation.

  • Rizi Ai
  • , Deepa Hammaker
  •  & Wei Wang

• Article
  05 April 2016 | Open Access

  Sialylation converts arthritogenic IgG into inhibitors of collagen-induced arthritis

  Post-translational modifications, such as glycosylation and sialylation, are thought to confer disease modifying effects on autoimmune-associated antibodies, including anti-citrullinated protein antibodies in rheumatoid arthritis. Here the authors show that sialylation converts arthritogenic IgG into inhibitors of collagen-induced arthritis in mice.

  • Yuhsuke Ohmi
  • , Wataru Ise
  •  & Koichi Furukawa

• Article
  25 September 2015 | Open Access

  CTRP6 is an endogenous complement regulator that can effectively treat induced arthritis

  The complement system contributes to chronic inflammatory diseases. Here the authors show that CRTP6 suppresses the alternative complement pathway and reverses rheumatoid arthritis in a mouse model of the disease.

  • Masanori A. Murayama
  • , Shigeru Kakuta
  •  & Yoichiro Iwakura

• Article
  25 June 2015 | Open Access

  IL-1 receptor antagonist-deficient mice develop autoimmune arthritis due to intrinsic activation of IL-17-producing CCR2⁺Vγ6⁺γδ T cells

  Control of γδ T-cell activation remains incompletely understood. Here the authors show that during autoimmune arthritis development αβ CD4⁺T cells recruit a subset of IL-17-producing γδ T cells to the joints, and that both components are essential to cause pathology in a mouse model of the disease.

  • Aoi Akitsu
  • , Harumichi Ishigame
  •  & Yoichiro Iwakura

• Article
  12 May 2015 | Open Access

  CD11c-mediated deletion of Flip promotes autoreactivity and inflammatory arthritis

  Dendritic cells are critical for initiation of immune responses and for induction of tolerance. Here the authors show that deletion of survival factor c-flip in CD11c-expressing cells subset perturbs CD8a⁺dendritic cell, NK and macrophage pools, and leads to development of autoimmune arthritis.

  • Qi-Quan Huang
  • , Harris Perlman
  •  & Richard M. Pope

• Article | 05 May 2015

  Crossreactivity to vinculin and microbes provides a molecular basis for HLA-based protection against rheumatoid arthritis

  Autoantibodies targeting citrunillated proteins are common in rheumatoid arthritis patients. Here the authors show that vinculin (a human protein) and some microbial proteins are recognized by these antibodies and by CD4⁺T cells, and this response is absent in patients carrying a protective HLA allele.

  • Jurgen van Heemst
  • , Diahann T. S. L. Jansen
  •  & René E. Toes

• Article
  03 April 2013 | Open Access

  A chronic model of arthritis supported by a strain-specific periarticular lymph node in BALB/c mice

  Mouse models of arthritis generally do not result in both chronic disease and autoantibody production—two key features of the human disease. Here the authors obtain both features by combining two common protocols, and find that disease severity is associated with the presence of a previously unidentified lymph node.

  • Uta Baddack
  • , Sven Hartmann
  •  & Gerd Müller