Filter By:

Journal Check one or more journals to show results from those journals only.

Choose more journals

Article type Check one or more article types to show results from those article types only.
Subject Check one or more subjects to show results from those subjects only.
Date Choose a date option to show results from those dates only.

Custom date range

Clear all filters
Sort by:
Showing 1–6 of 6 results
Advanced filters: Author: Simon Rauber Clear advanced filters
  • Here the authors use positron emission tomography to visualize fibroblasts in patients with arthritis and combined with spatial transcriptomic data show that these cells undergo a phenotypic shift upon resolution of inflammation. A CD200+DKK3+ fibroblast subset promotes this resolution by inhibiting tumor necrosis factor and interleukin-17A.

    • Simon Rauber
    • Hashem Mohammadian
    • Andreas Ramming
    Research
    Nature Immunology
    Volume: 25, P: 682-692
  • Microglial activation is critical for coordinating the immune response during neuroinflammation. Here, the authors demonstrate that the CD83 molecule intrinsically modulates microglial activity and restrains inflammatory processes in experimental autoimmune encephalomyelitis.

    • Pia Sinner
    • Katrin Peckert-Maier
    • Andreas B. Wild
    ResearchOpen Access
    Nature Communications
    Volume: 14, P: 1-17
  • Uncontrolled activation of fibroblasts contributes to tissue fibrosis and organ dysfunction. Here the authors demonstrate that the epigenetic control of autophagy is disturbed by a TGFβ-dependent downregulation of MYST1 in systemic sclerosis patients. Restoration of the epigenetic control of autophagy reduces fibroblast activation and ameliorates fibrotic tissue remodeling.

    • Ariella Zehender
    • Yi-Nan Li
    • Jörg H. W. Distler
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-19
  • The transcription factor PU.1 is an essential regulator of the pro-fibrotic gene expression program in fibroblasts; PU.1 expression is upregulated in various fibrotic diseases, whereas inactivation of PU.1 induces regression of fibrosis in a number of organs.

    • Thomas Wohlfahrt
    • Simon Rauber
    • Andreas Ramming
    Research
    Nature
    Volume: 566, P: 344-349
  • Number of IL-9-expressing ILC2s are elevated in patients with inflammatory arthritis during remission, and these cells are critical in mice for the resolution of inflammatory arthritis via regulatory T cell induction. Delivery of DNA minicircles encoding IL-9 into inflamed joints ameliorates mouse experimental arthritis, suggesting possible therapeutic applications.

    • Simon Rauber
    • Markus Luber
    • Andreas Ramming
    Research
    Nature Medicine
    Volume: 23, P: 938-944