Abstract
BackgroundThe immune mechanism was shown to be involved in the development of adenomyosis. The aim of the current study was to evaluate the expression of the immune checkpoints B7-H2, B7-H3, B7-H4 and PD-L2 in adenomyosis and to explore the effect of mifepristone on the expression of these immune checkpoints.MethodsThe expression of B7-H2, B7-H3, B7-H4 and PD-L2 in normal endometria and adenomyosis patient samples treated with or without mifepristone was determined by immunohistochemistry analysis.ResultsIn adenomyosis patient samples, the expression of B7-H2, B7-H3 and B7-H4 was increased in the eutopic and ectopic endometria compared with normal endometria, both in the proliferative and secretory phases. Moreover, the expression of B7-H2 and B7-H3 was higher in adenomyotic lesions than in the corresponding eutopic endometria, both in the proliferative and secretory phases. The expression of PD-L2 was higher in adenomyotic lesions than in normal endometria in both the proliferative and secretory phases. In the secretory phase but not the proliferative phase, the expression of B7-H4 and PD-L2 in adenomyotic lesions was significantly higher than that in the corresponding eutopic endometria. In normal endometria and eutopic endometria, the expression of B7-H4 was elevated in the proliferative phase compared with that in the secretory phase, while in the ectopic endometria, B7-H4 expression was decreased in the proliferative phase compared with the secretory phase. In addition, the expression of B7-H2, B7-H3, B7-H4 and PD-L2 was significantly decreased in adenomyosis tissues after treatment with mifepristone.ConclusionsThe expression of the immune checkpoint proteins B7-H2, B7-H3, B7-H4 and PD-L2 is upregulated in adenomyosis tissues and is downregulated with mifepristone treatment. The data suggest that B7 immunomodulatory molecules are involved in the pathophysiology of adenomyosis.
Highlights
The immune mechanism was shown to be involved in the development of adenomyosis
The results showed that the eutopic and ectopic endometrium of adenomyosis patients treated with mifepristone showed significantly lower expression of B7-H2, B7-H3, B7-H4 and PD-L2 protein compared with that of adenomyosis patients without mifepristone treatment, both in the proliferative phase and in the secretory phase (Figs. 1, 2, 3 and 4g-j all P < 0.01)
Since there is little knowledge of the correlation between the B7 family and adenomyosis, our study explored the expression of B7-H2, B7-H3, B7-H4 and PD-L2 in adenomyosis patients with and without mifepristone treatment
Summary
The immune mechanism was shown to be involved in the development of adenomyosis. The aim of the current study was to evaluate the expression of the immune checkpoints B7-H2, B7-H3, B7-H4 and PD-L2 in adenomyosis and to explore the effect of mifepristone on the expression of these immune checkpoints. Qin et al Reprod Biol Endocrinol (2021) 19:114 systemic and local immune alterations exist in women affected by adenomyosis, with the coexistence of changes in inflammatory and anti-inflammatory signals [5]. This underscores the immune contributions to the disease. The newly identified B7 proteins B7-H2, B7-H3, B7-H4 and programmed death ligand 2 (PD-L2, CD273, B7-DC) have attracted increasing attention These cosignaling molecules provide critical positive signals that stimulate T cell growth, upregulate cytokine production and promote T cell differentiation and contribute key negative signals to limit, terminate and/or attenuate T cell responses [6, 7]. We wondered whether altered expression of these B7 family members could be observed in adenomyosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
