RORγt-specific transcriptional interactomic inhibition suppresses autoimmunity associated with TH17 cells

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Pharmacological inhibition of RORγt suppresses the Th17 pathway and alleviates arthritis in vivo

Retinoic acid receptor-related-orphan-receptor-C (RORγt) is the key transcription factor that is driving the differentiation of IL-17 producing T-helper 17 (Th17) cells that are implicated in the pathology of various autoimmune and inflammatory diseases. Based on the importance of RORγt in promoting Th17-driven pathology, there is considerable interest to develop low-molecular-weight compounds ...

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FOXP3 and RORγt: transcriptional regulation of Treg and Th17.

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RORγt and RORα signature genes in human Th17 cells

RORγt and RORα are transcription factors of the RAR-related orphan nuclear receptor (ROR) family. They are expressed in Th17 cells and have been suggested to play a role in Th17 differentiation. Although RORγt signature genes have been characterized in mouse Th17 cells, detailed information on its transcriptional control in human Th17 cells is limited and even less is known about RORα signature...

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Interleukin (IL) 17-producing T helper (T(H)17) cells have been selected through evolution for their ability to control fungal and bacterial infections. It is also firmly established that their aberrant generation and activation results in autoimmune conditions. Using a characterized potent and selective small molecule inhibitor, we show that the bromodomain and extra-terminal domain (BET) fami...

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Th17 Cells in Immunity and Autoimmunity

Th17 and IL-17 play important roles in the clearance of extracellular bacterial and fungal infections. However, strong evidence also implicates the Th17 lineage in several autoimmune disorders including multiple sclerosis, psoriasis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and asthma. The Th17 subset has also been connected with type I diabetes, although ...

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ژورنال

عنوان ژورنال: Proceedings of the National Academy of Sciences

سال: 2014

ISSN: 0027-8424,1091-6490

DOI: 10.1073/pnas.1413687112