RBPJ Controls Development of Pathogenic Th17 Cells by Regulating IL-23 Receptor Expression

• Published in: Cell reports (Cambridge) Vol. 16; no. 2; pp. 392 - 404
• Main Authors: Meyer zu Horste, Gerd, Wu, Chuan, Wang, Chao, Cong, Le, Pawlak, Mathias, Lee, Youjin, Elyaman, Wassim, Xiao, Sheng, Regev, Aviv, Kuchroo, Vijay K.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 12.07.2016; Elsevier
• Subjects: Animals; Binding Sites; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - metabolism; Gene Expression; Gene Expression Regulation - immunology; IL-23R; Immunoglobulin J Recombination Signal Sequence-Binding Protein - physiology; Interleukin-10 - biosynthesis; Mice, 129 Strain; Mice, Inbred C57BL; Notch; Nuclear Receptor Subfamily 1, Group F, Member 3 - metabolism; pathogenicity; Promoter Regions, Genetic; Protein Binding; Proto-Oncogene Proteins c-maf - physiology; RBPJ; Receptors, Interleukin - genetics; Receptors, Interleukin - metabolism; Th17 cells; Th17 Cells - metabolism; Transcriptional Activation; pathogenicity; IL-23R; RBPJ; Notch; Th17 cells

Interleukin-17 (IL-17)-producing helper T cells (Th17 cells) play an important role in autoimmune diseases. However, not all Th17 cells induce tissue inflammation or autoimmunity. Th17 cells require IL-23 receptor (IL-23R) signaling to become pathogenic. The transcriptional mechanisms controlling th...