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Updated: Jun 3, 2026

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
Published on: October 25, 2024
Cyclooxygenase-2 regulates Th17 cell differentiation during allergic lung inflammation
Hong Li1, J Alyce Bradbury, Ryan T Dackor
1Laboratories of Respiratory Biology; National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
Cyclooxygenase-2 (COX-2) is crucial for Th17 cell differentiation in allergic lung inflammation. Its metabolites, PGI(2) and PGF(2α), regulate these pro-inflammatory cells via specific receptors.
Area of Science:
- Immunology
- Inflammation Research
- T cell Biology
Background:
- Th17 cells are key drivers of allergic responses.
- The role of cyclooxygenase (COX)-derived eicosanoids in Th17 cell regulation during allergic lung inflammation remains unclear.
Purpose of the Study:
- To investigate the role of COX metabolites in regulating Th17 cell differentiation and function.
- To elucidate the specific mechanisms by which COX-2 influences allergic lung inflammation.
Main Methods:
- Utilized a murine model of ovalbumin-induced allergic lung inflammation.
- Employed in vitro Th17 differentiation assays with COX-1(-/-), COX-2(-/-), and wild-type cells.
- Analyzed Th17 cell differentiation, Stat3 phosphorylation, and RORγt expression.
- Investigated the effects of specific prostaglandins (PGs), inhibitors, and siRNA knockdown.
Main Results:
- COX-2 deficiency significantly impaired Th17 cell differentiation in vivo and in vitro.
- COX-2(-/-) T cells showed reduced Stat3 phosphorylation and RORγt expression.
- Synthetic PGF(2α) and PGI(2) restored Th17 differentiation in COX-2 deficient cells.
- Targeting PGF(2α) and PGI(2) receptors reduced Th17 differentiation.
Conclusions:
- COX-2 is essential for Th17 cell differentiation in allergic lung inflammation.
- Autocrine signaling of PGI(2) and PGF(2α) through their receptors mediates COX-2's effect on Th17 cells.
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