Prostaglandin D2 amplifies lupus disease through basophil accumulation in lymphoid organs

Christophe Pellefigues, Barbara Dema, Yasmine Lamri, Fanny Saidoune, Nathalie Chavarot, Charlotte Lohéac, Emeline Pacreau, Michael Dussiot, Caroline Bidault, Florian Marquet, Mathieu Jablonski, Jonathan M. Chemouny, Fanny Jouan, Antoine Dossier, Marie-Paule Chauveheid, Delphine Gobert, Thomas Papo, Hajime Karasuyama, Karim Sacré, Eric Daugas and Nicolas Charles ()
Additional contact information
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
Fanny Jouan: Université Paris Diderot
Antoine Dossier: Université Paris Diderot
Marie-Paule Chauveheid: Université Paris Diderot
Delphine Gobert: Université Paris Diderot
Thomas Papo: Université Paris Diderot
Hajime Karasuyama: Tokyo Medical and Dental University (TMDU)
Karim Sacré: Université Paris Diderot
Eric Daugas: Université Paris Diderot
Nicolas Charles: Université Paris Diderot

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: 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.

Date: 2018
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03129-8

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DOI: 10.1038/s41467-018-03129-8

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