Mifepristone Increases the Cytotoxicity of Uterine Natural Killer Cells by Acting as a Glucocorticoid Antagonist via ERK Activation

Authors: Yuezhou Chen, Yan Wang, Yaling Zhuang, Feng Zhou, Lili Huang

DOI: 10.1371/journal.pone.0036413

Abstract Summary

Mifepristone enhances uterine natural killer cell cytotoxicity by blocking glucocorticoid activity, not progesterone. The drug increases perforin expression and activates the ERK1/2 signaling pathway, effects reversed by cortisol. This glucocorticoid antagonism mechanism reveals how mifepristone boosts immune function in the uterus, offering new insights into its therapeutic applications.

Why Brain? 🧠

Mifepristone enhances uterine natural killer cell killing ability by blocking cortisol effects through ERK pathway activation, revealing a key immune mechanism beyond its known progesterone-blocking action.

The image is AI-generated for illustrative purposes only. Courtesy of Midjourney.