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. 2021 Jun 14;22(3):125–140. doi: 10.1038/s41435-021-00139-3

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — A Glucocorticoids (GC) in presence of specific cytokines (IL-12, IL-15, and IL-18) induce the expression of inhibitory receptor PD-1 on CD56^bright NK cells, which is responsible for immunosupression in the tumor microenvironment. B GCs reduce the expression of perforins, granzymes, and IFN-γ by epigenetic modifications, which decrease the cytotoxic effect of NK cell. Glucocorticoids also reduce the expression of integrin lymphocyte function-associated antigen 1 (LFA-1) on the surface of NK cell, this hampers the attachment of NK cell to target cell. C Estradiol (E2) induces uterine natural killer cells (uNK cells) to secrete chemokine (C-C motif) ligand 2 (CCL2), which results endometrium angiogenesis. In early stage of pregnancy, estradiol (E2) or progesterone (P4) increases the expression of L-selectin and α4 integrin on circulatory CD56^bright NK cells. D Low concentration of glucocorticoids reduces histone acetylation in the promoter region of genes PRF1 (encodes perforin) and GZMB (encodes granzyme B) thereby reduces the cytolytic activity of NK cells; and prime NK cells for the production of pro-inflammatory cytokines by augmenting acetylation in the enhancer or promoter region of genes IFNG and IL-6. (Figure created with BioRender.com).