Regulatory effects of dexamethasone on NK and T cell immunity

被引:31
|
作者
Chen, Liying [1 ]
Jondal, Mikael [1 ]
Yakimchuk, Konstantin [2 ]
机构
[1] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, S-17177 Stockholm, Sweden
[2] Karolinska Inst, Novum, Dept Biosci & Nutr, S-14183 Huddinge, Sweden
关键词
Glucocorticoids; Dexamethasone; NK cells; T cells; Regulatory T cells; GLUCOCORTICOID-RECEPTOR; FOXP3; EXPRESSION; OLD DRUGS; MECHANISMS; CORTICOSTEROIDS; STRESS; INTERLEUKIN-4; TRANSCRIPTION; NEUTROPHILS; ACTIVATION;
D O I
10.1007/s10787-017-0418-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Glucocorticoids (GCs) act via the intracellular glucocorticoid receptor (GR), which can regulate the expression of target genes. With regard to the immune system, GCs may affect both innate and adaptive immunity. Our study analyzed the immunoregulatory effects of dexamethasone (Dex) treatment on splenic T, Treg, NK and NKT cells by treating C57Bl6 mice with various doses of Dex. We observed that treatment with Dex decreased the number of NK cells in the spleen and suppressed their activity. In particular, the expression of both Ly49G and NKG2D receptors was decreased by Dex. However, Dex did not affect the population of NKT cells. With regard to splenic T cells, our results show a dose-dependent reduction in CD3(+), CD4(+), CD8(+), CD44(+) and CD8(+)CD122(+) T cells, but a stimulatory effect on CD4(+)CD25(+) regulatory T cells by Dex treatment. In addition, treatment with Dex suppressed anti-tumor immune response in a mouse EG7 tumor model. We conclude that Dex may suppress both T- and NK-mediated immunity.
引用
收藏
页码:1331 / 1338
页数:8
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