Prostaglandin D2 amplifies lupus disease through basophil accumulation in lymphoid organs View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

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, Nicolas Charles

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. More... »

PAGES

725

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41467-018-03129-8

DOI

http://dx.doi.org/10.1038/s41467-018-03129-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1101045808

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29463843


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