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? đź§
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.
