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| Status |
Public on Feb 23, 2021 |
| Title |
T cell-intrinsic prostaglandin E2-EP2/EP4 signaling is critical in pathogenic Th17 cell-driven inflammation |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
|
| Summary |
IL-23 induces ptgs2 encoding cyclooxygenase 2 in Th17 cells and produces PGE2, which acts back on PGE2 receptors EP2 and EP4 in these cells and enhances IL-23-induced expression of an IL-23 receptor subunit gene, Il23r, by activating STAT3, CREB1 and NF-κB through cAMP-protein kinase A signaling. This PGE2 signaling also induces expression of various inflammation-related genes, which possibly function in Th17 cell-mediated pathology. Combined deletion of EP2 and EP4 selectively in T cells suppressed accumulation of IL-17A+ and IL-17A+IFN-γ+ pathogenic Th17 cells and abolished skin inflammation in IL-23-induced psoriasis mouse model. Analysis of human psoriatic skin biopsies shows positive correlation between PGE2 signaling and the IL-23/Th17 pathway.
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| Overall design |
IL-23 mobilizes T cell-intrinsic PGE2-EP2/EP4 signaling, which is critical in IL-23-induced pathogenic Th17 cell generation. Combined blockade of EP2 and EP4 suppressed IL-23-induced skin inflammation, suggesting this pathway as potential therapeutic target of Th17-mediated diseases.
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| Contributor(s) |
Lee J, Aoki T |
| Citation(s) |
29935220 |
| Submission date |
Feb 22, 2021 |
| Last update date |
Feb 26, 2021 |
| Contact name |
Jinju Lee |
| E-mail(s) |
jj3168@gmail.com
|
| Organization name |
University of Ulsan
|
| Street address |
88, Olympic-ro 43-gil, Songpa-gu
|
| City |
Seoul |
| ZIP/Postal code |
05505 |
| Country |
South Korea |
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| Platforms (1) |
| GPL13912 |
Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Feature Number version) |
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| Samples (12)
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| Relations |
| BioProject |
PRJNA703988 |
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