The β2-adrenergic biased agonist nebivolol inhibits the development of Th17 and the response of memory Th17 cells in an NF-κB-dependent manner
The findings demonstrate that nebivolol acts through a β<sub>2</sub>-AR-mediated signaling pathway, as a distinctive anti-inflammatory agent capable of selectively shifting Th17 cells and suppressing the phosphorylation of NF-κB. This highlights nebivolol's potential for therapeutic interventions in chronic autoimmune conditions with elevated IL-17A levels.
Authors
- Mehri Hajiaghayi
- Samuel R. Little (ORCID: https://orcid.org/0000-0003-4075-6083)
- Steve C. C. Shih (ORCID: https://orcid.org/0000-0003-3540-0808)
- Peter J. Darlington (ORCID: https://orcid.org/0000-0002-7976-9108)
- Fatemeh Gholizadeh (ORCID: https://orcid.org/0000-0002-1518-4629)
- Niloufar Rahbari
- Eric Han
- Isabella Ardila
- Kasra Tehranimeh
- Carolina Naranjo
Institutions
- Concordia University (CA)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2024-10-09
- DOI
- https://doi.org/10.3389/fimmu.2024.1446424
- Citations
- 1
- Primary Topic
- T-cell and B-cell Immunology
- Type
- article
- Field-Weighted Citation Impact
- 0.24
Funders
- Natural Sciences and Engineering Research Council of Canada
- Fonds de recherche du Québec – Nature et technologies