Prostaglandin E2–EP4 signaling promotes immune inflammation through TH1 cell differentiation and TH17 cell expansion

• Published in: Nature medicine Vol. 15; no. 6; pp. 633 - 640
• Main Authors: Yao, Chengcan, Sakata, Daiji, Esaki, Yoshiyasu, Li, Youxian, Matsuoka, Toshiyuki, Kuroiwa, Kenji, Sugimoto, Yukihiko, Narumiya, Shuh
• Format: Journal Article
• Language: English
• Published: New York Nature Publishing Group US 01.06.2009; Nature Publishing Group
• Subjects: Animal models; Animals; Autoimmune diseases; Biomedical and Life Sciences; Biomedicine; Cancer Research; Cell differentiation; Cell Differentiation - immunology; Cell growth; Dendritic Cells - immunology; Dendritic Cells - metabolism; Dermatitis, Contact - immunology; Dinoprostone - immunology; Dinoprostone - metabolism; Encephalomyelitis, Autoimmune, Experimental - immunology; Hypersensitivity; Immune system; Infectious Diseases; Inflammation - immunology; Inflammation - metabolism; Interleukin-17 - immunology; Interleukin-23 - biosynthesis; Interleukin-23 - immunology; Lipids; Lymph nodes; Lymphocytes; Metabolic Diseases; Mice; Molecular Medicine; Neurosciences; Proteins; Receptors, Prostaglandin E - immunology; Receptors, Prostaglandin E - metabolism; Receptors, Prostaglandin E, EP4 Subtype; Rheumatoid arthritis; Signal Transduction - immunology; Skin diseases; Th1 Cells - immunology; Th1 Cells - metabolism

Prostaglandins play a key role in inflammation in a variety of settings. Now, Shuh Narumiya and colleagues show that prostaglandin E2 drives the production of inflammatory T helper cells, and that this can be blocked by inhibiting its EP4 receptor subtype. EP4 inhibitors were also effective at inhib...