2014
DOI: 10.1016/j.tips.2014.07.006
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Targeting Th17 cells in autoimmune diseases

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Cited by 307 publications
(217 citation statements)
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References 61 publications
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“…Hence, the effector subtype is called Th 17 and it orchestrates critical roles in facilitating the recruitment of innate immune cells, such as macrophages, to infected tissues. The dysregulation of Th 17 leads to major autoimmune diseases and, on some occasions, cancer (Su et al, 2014;Yang et al, 2014). Although there are numerous works, lately, that characterize novel details about individual factors, large-scale global response studies are still limited.…”
Section: Introductionmentioning
confidence: 99%
“…Hence, the effector subtype is called Th 17 and it orchestrates critical roles in facilitating the recruitment of innate immune cells, such as macrophages, to infected tissues. The dysregulation of Th 17 leads to major autoimmune diseases and, on some occasions, cancer (Su et al, 2014;Yang et al, 2014). Although there are numerous works, lately, that characterize novel details about individual factors, large-scale global response studies are still limited.…”
Section: Introductionmentioning
confidence: 99%
“…5 RORt inhibitors has potential utility in reducing the activity of Th17 cells and therefore can be developed as therapeutic agents for the treatment of Th17-mediated autoimmune diseases. [7][8][9][10][11][12][13] A few small molecule inhibitors against RORt have been reported in literature. 14 Digoxin, 15 SR1001 16 and Ursolic acid 17 were firstly reported to inhibit RORt and ameliorate EAE in mice via intraperitoneal administration.…”
Section: Introductionmentioning
confidence: 99%
“…58 Although Th17 cells have been identified as a new CD4 C T subset based on the expression of the critical transcription factor retinoic acid receptor-related orphan receptor-gt (RORgt) and cytokines in the IL-17 family, 59 there is evidence indicating that BCL6 and Ncor2 are also 2 important transcription factors in Th17 cell differentiation. In a recent study, retinoic acid (RA) was shown to induce miRNA-10a expression, which directly targets sequences in the 3 0 -UTR of BCL6 mRNA and downregulates BCL6 expression.…”
Section: Th17 Cellsmentioning
confidence: 99%