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Prostaglandin D2 amplifies lupus disease through basophil accumulation in lymphoid organs

Author

Listed:
  • Christophe Pellefigues

    (Université Paris Diderot)

  • Barbara Dema

    (Université Paris Diderot)

  • Yasmine Lamri

    (Université Paris Diderot)

  • Fanny Saidoune

    (Université Paris Diderot)

  • Nathalie Chavarot

    (Université Paris Diderot)

  • Charlotte Lohéac

    (Université Paris Diderot)

  • Emeline Pacreau

    (Université Paris Diderot)

  • Michael Dussiot

    (Institut Imagine)

  • Caroline Bidault

    (Université Paris Diderot)

  • Florian Marquet

    (Université Paris Diderot)

  • Mathieu Jablonski

    (Université Paris Diderot)

  • Jonathan M. Chemouny

    (Université Paris Diderot
    Université Paris Diderot)

  • Fanny Jouan

    (Université Paris Diderot
    Université Paris Diderot)

  • Antoine Dossier

    (Université Paris Diderot)

  • Marie-Paule Chauveheid

    (Université Paris Diderot)

  • Delphine Gobert

    (Université Paris Diderot)

  • Thomas Papo

    (Université Paris Diderot
    Université Paris Diderot)

  • Hajime Karasuyama

    (Tokyo Medical and Dental University (TMDU))

  • Karim Sacré

    (Université Paris Diderot
    Université Paris Diderot)

  • Eric Daugas

    (Université Paris Diderot
    Université Paris Diderot)

  • Nicolas Charles

    (Université Paris Diderot)

Abstract

In systemic lupus erythematosus (SLE), autoantibody production can lead to kidney damage and failure, known as lupus nephritis. Basophils amplify the synthesis of autoantibodies by accumulating in secondary lymphoid organs. Here, we show a role for prostaglandin D2 (PGD2) in the pathophysiology of SLE. Patients with SLE have increased expression of PGD2 receptors (PTGDR) on blood basophils and increased concentration of PGD2 metabolites in plasma. Through an autocrine mechanism dependent on both PTGDRs, PGD2 induces the externalization of CXCR4 on basophils, both in humans and mice, driving accumulation in secondary lymphoid organs. Although PGD2 can accelerate basophil-dependent disease, antagonizing PTGDRs in mice reduces lupus-like disease in spontaneous and induced mouse models. Our study identifies the PGD2/PTGDR axis as a ready-to-use therapeutic modality in SLE.

Suggested Citation

  • Christophe Pellefigues & Barbara Dema & Yasmine Lamri & Fanny Saidoune & Nathalie Chavarot & Charlotte Lohéac & Emeline Pacreau & Michael Dussiot & Caroline Bidault & Florian Marquet & Mathieu Jablons, 2018. "Prostaglandin D2 amplifies lupus disease through basophil accumulation in lymphoid organs," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03129-8
    DOI: 10.1038/s41467-018-03129-8
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