Shirshev S V, Nekrasova I V, Gorbunova O L, Orlova E G
Institute of Ecology and Genetics of Microorganisms, Perm' Federal Research Center of Ural Division of Russian Academy of Sciences, Perm', Russia.
Bull Exp Biol Med. 2019 May;167(1):57-61. doi: 10.1007/s10517-019-04460-w. Epub 2019 Jun 8.
We studied the effect of estriol, chorionic gonadotropin, oncostatin M, and hormone-cytokine combinations on the expression of recombinase RAG-1 in T-regulatory (Treg) and T helper 17 (Th17) lymphocytes. It was found that estriol in a concentration corresponding to the first trimester of pregnancy increased the level of Treg (CD4FoxP3) cells and suppressed the formation of Th17 (CD4RORC) lymphocytes. This effect was nor observed after individual administration of chorionic gonadotropin and oncostatin M, but some combinations of the studied hormones with oncostatin M increased the percentage of CD4FOXP3 cells. In the presence of oncostatin M, the studied hormones enhanced the expression of RAG-1 in CD4FoxP3 cells, but not in CD4RORC cells, thereby initiating of Treg T-cell receptor (TCR) revision. The mechanisms of hormone cytokine control of induction of the immune tolerance during pregnancy are discussed.
我们研究了雌三醇、绒毛膜促性腺激素、制瘤素M以及激素 - 细胞因子组合对调节性T（Treg）淋巴细胞和辅助性T细胞17（Th17）中重组酶RAG - 1表达的影响。研究发现，与妊娠早期浓度相当的雌三醇可提高Treg（CD4FoxP3）细胞水平，并抑制Th17（CD4RORC）淋巴细胞的形成。单独给予绒毛膜促性腺激素和制瘤素M后未观察到这种效应，但所研究的激素与制瘤素M的某些组合可增加CD4FOXP3细胞的百分比。在制瘤素M存在的情况下，所研究的激素增强了CD4FoxP3细胞中RAG - 1的表达，但未增强CD4RORC细胞中的表达，从而启动了Treg T细胞受体（TCR）的修正。本文讨论了孕期激素细胞因子控制免疫耐受诱导的机制。
