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dc.contributor.authorPark, Tae-Yoonen_US
dc.contributor.authorJang, Yongwooen_US
dc.contributor.authorKim, Woorien_US
dc.contributor.authorShin, Joonen_US
dc.contributor.authorToh, Hui Tingen_US
dc.contributor.authorKim, Chun-Hyungen_US
dc.contributor.authorYoon, Ho Supen_US
dc.contributor.authorLeblanc, Pierreen_US
dc.contributor.authorKim, Kwang-Sooen_US
dc.identifier.citationPark, T.-Y., Jang, Y., Kim, W., Shin, J., Toh, H. T., Kim, C.-H., . . . Kim, K.-S. (2019). Chloroquine modulates inflammatory autoimmune responses through Nurr1 in autoimmune diseases. Scientific Reports, 9(1), 15559-. doi:10.1038/s41598-019-52085-wen_US
dc.description.abstractFor over a half-century the anti-malarial drug chloroquine (CQ) has been used as a therapeutic agent, alone or in combination, to treat autoimmune diseases. However, neither the underlying mechanism(s) of action nor their molecular target(s) are well defined. The orphan nuclear receptor Nurr1 (also known as NR4A2) is an essential transcription factor affecting the development and maintenance of midbrain dopaminergic neurons. In this study, using in vitro T cell differentiation models, we demonstrate that CQ activates TREG cell differentiation and induces Foxp3 gene expression in a Nurr1-dependent manner. Remarkably, CQ appears to induce Nurr1 function by two distinct mechanisms: firstly, by direct binding to Nurr1's ligand-binding domain and promoting its transcriptional activity and secondly by upregulation of Nurr1 expression through the CREB signaling pathway. In contrast, CQ suppressed gene expression and differentiation of pathogenic TH17 cells. Importantly, using a valid animal model of inflammatory bowel disease (IBD), we demonstrated that CQ promotes Foxp3 expression and differentiation of TREG cells in a Nurr1-dependent manner, leading to significant improvement of IBD-related symptoms. Taken together, these data suggest that CQ ameliorates autoimmune diseases via regulating Nurr1 function/expression and that Nurr1 is a promising target for developing effective therapeutics of human inflammatory autoimmune diseases.en_US
dc.relation.ispartofScientific Reportsen_US
dc.rights© 2019 The Author(s). This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Te images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit
dc.subjectScience::Biological sciencesen_US
dc.titleChloroquine modulates inflammatory autoimmune responses through Nurr1 in autoimmune diseasesen_US
dc.typeJournal Articleen
dc.contributor.schoolSchool of Biological Sciencesen_US
dc.description.versionPublished versionen_US
dc.subject.keywordsChloroquine (CQ)en_US
dc.subject.keywordsInflammatory Autoimmune Responsesen_US
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