期刊
JOURNAL OF IMMUNOLOGY
卷 175, 期 10, 页码 6509-6516出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.10.6509
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- NCI NIH HHS [CA23108] Funding Source: Medline
- NIAID NIH HHS [AI51877] Funding Source: Medline
The objective of this study was to examine the effects of sex hormones on IL-10-mediated responses by uterine epithelial cells. The mRNA expression and secretion of human beta-defensin-2 and CXCL8 by uterine epithelial cells was examined following stimulation with IL-1 beta in the presence of estradiol or progesterone. Estradiol inhibited the IL-1 beta-mediated mRNA expression and secretion of human beta-defensin-2 and CXCL8 by uterine epithelial cells while progesterone had no effect. Inhibition of the IL-10-mediated response by estradiol was dose dependent, with maximal inhibition observed using 10(-7) to 10(-10) M, and was shown to be mediated through the estrogen receptor because addition of a pure estrogen receptor antagonist abrogated this effect. The mechanism by which estradiol inhibits IL-1 beta-mediated responses by uterine epithelial cells appears to be the down-modulation of the IL-1R type 1, thereby reducing the uterine epithelial cell's ability to respond to IL-1 beta. These results suggest that the inhibitory effect of estradiol on IL-10-mediated inflammatory responses by uterine epithelial cells indicates a link between the endocrine and immune systems and may be crucial for dampening proinflammatory responses during the time of ovulation or pregnancy.
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