Details

Autor(en) / Beteiligte

• Pellefigues, Christophe
• Dema, Barbara
• Lamri, Yasmine
• Saidoune, Fanny
• Chavarot, Nathalie
• Lohéac, Charlotte
• Pacreau, Emeline
• Dussiot, Michael
• Bidault, Caroline
• Marquet, Florian
• Jablonski, Mathieu
• Chemouny, Jonathan M
• Jouan, Fanny
• Dossier, Antoine
• Chauveheid, Marie-Paule
• Gobert, Delphine
• Papo, Thomas
• Karasuyama, Hajime
• Sacré, Karim
• Daugas, Eric
• Charles, Nicolas

Titel

Prostaglandin D 2 amplifies lupus disease through basophil accumulation in lymphoid organs

Ist Teil von

• Nature communications, 2018-02, Vol.9 (1), p.725

Ort / Verlag

England

Erscheinungsjahr

2018

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• 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 D (PGD ) in the pathophysiology of SLE. Patients with SLE have increased expression of PGD receptors (PTGDR) on blood basophils and increased concentration of PGD metabolites in plasma. Through an autocrine mechanism dependent on both PTGDRs, PGD induces the externalization of CXCR4 on basophils, both in humans and mice, driving accumulation in secondary lymphoid organs. Although PGD can accelerate basophil-dependent disease, antagonizing PTGDRs in mice reduces lupus-like disease in spontaneous and induced mouse models. Our study identifies the PGD /PTGDR axis as a ready-to-use therapeutic modality in SLE.