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. 2021 Apr 29;11(5):659. doi: 10.3390/biom11050659

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Cardiac glycosides at low nanomolar concentrations activate RORγt, whereas at high concentrations they cause RORγt transcriptional inhibition. This influences the production of interleukins (IL) 17 and 22 in T-helper cells expressing IL-17 (Th17). The interleukins promote autoimmune diseases by activating immune cells, such as follicular B-helper T cells (TFH), type 1 and type 2 T-helper cells (Th1, Th2), type 1 regulatory T cells (TR1), and regulatory T cells (Treg). These cells produce IL, interferon γ (IFNγ), or transforming growth factor-beta (TGF-β).