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Immune modules to guide diagnosis and personalized treatment of inflammatory skin diseases

Author

Listed:
  • Teofila Seremet

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Jeremy Di Domizio

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Antoine Girardin

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Ahmad Yatim

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Raphael Jenelten

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Francesco Messina

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Fanny Saidoune

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Christoph Schlapbach

    (University of Bern)

  • Sofia Bogiatzi

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Frederic Minisini

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Natalie Garzorz-Stark

    (University of Freiburg)

  • Matthieu Leuenberger

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Héloise Wüthrich

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Maxime Vernez

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Daniel Hohl

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Stefanie Eyerich

    (University of Freiburg)

  • Kilian Eyerich

    (University of Freiburg)

  • Emmanuella Guenova

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Carle Paul

    (CHU Toulouse)

  • Raphael Gottardo

    (and SIB)

  • Curdin Conrad

    (Lausanne University Hospital CHUV and University of Lausanne)

  • Michel Gilliet

    (Lausanne University Hospital CHUV and University of Lausanne)

Abstract

Previous advances have identified immune pathways associated with inflammatory skin diseases, leading to the development of targeted therapies. However, there is a lack of molecular approaches that delineate these pathways at the individual patient level for personalized diagnostic and therapeutic guidance. Here, we conduct a cross-comparison of expression profiles from multiple inflammatory skin diseases to identify gene modules defining relevant immune pathways. Seven modules are identified, representing key immune pathways: Th17, Th2, Th1, Type I IFNs, neutrophilic, macrophagic, and eosinophilic. These modules allow the development of a molecular map with high diagnostic efficacy for inflammatory skin diseases and clinico-pathologically undetermined cases. Aligning dominant modules with treatment targets offers a rational framework for treatment selection, improving response rates in both treatment-naïve patients and non-responders to targeted therapies. Overall, our approach offers precision medicine for inflammatory skin diseases, utilizing transcriptional modules to support diagnosis and guide personalized treatment selection.

Suggested Citation

  • Teofila Seremet & Jeremy Di Domizio & Antoine Girardin & Ahmad Yatim & Raphael Jenelten & Francesco Messina & Fanny Saidoune & Christoph Schlapbach & Sofia Bogiatzi & Frederic Minisini & Natalie Garzo, 2024. "Immune modules to guide diagnosis and personalized treatment of inflammatory skin diseases," Nature Communications, Nature, vol. 15(1), pages 1-12, December.
  • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-54559-6
    DOI: 10.1038/s41467-024-54559-6
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    References listed on IDEAS

    as
    1. A. Schäbitz & C. Hillig & M. Mubarak & M. Jargosch & A. Farnoud & E. Scala & N. Kurzen & A. C. Pilz & N. Bhalla & J. Thomas & M. Stahle & T. Biedermann & C. B. Schmidt-Weber & F. Theis & N. Garzorz-St, 2022. "Spatial transcriptomics landscape of lesions from non-communicable inflammatory skin diseases," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
    2. Curdin Conrad & Jeremy Di Domizio & Alessio Mylonas & Cyrine Belkhodja & Olivier Demaria & Alexander A. Navarini & Anne-Karine Lapointe & Lars E. French & Maxime Vernez & Michel Gilliet, 2018. "TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis," Nature Communications, Nature, vol. 9(1), pages 1-11, December.
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