Le mardi 14 avril 2026, Madame Marlyne SQUATRITO, titulaire d'un d’un Master en sciences biomédicales à finalité recherche interdisciplinaire et d'un Certificat de formation à la recherche en sciences biomédicales et pharmaceutiques, présentera l'examen en vue de l'obtention du grade de Doctorat en sciences biomédicales et pharmaceutiques, sous la direction de Madame Carine MUNAUT. 

Cette épreuve consistera en la défense publique d'une thèse intitulée : "Experimental study of fertility alterations, immune microenvironment changes, and S1P pathway targeting in a murine model of adenomyosis". 

Le jury sera composé de :

Michael HERFS (Président), Nathalie JACOBS (Secrétaire), Mathilde BOURDON (Hôp. Cochin), Laurent DE LANDSHEERE, Patrick HENRIET (UCLouvain), Carine MUNAUT, Laure NOEL.

Résumé de la thèse

A comprehensive understanding of the mechanisms by which adenomyosis leads to infertility remains incomplete. This pathology, characterized by the invasion of endometrial tissue into the myometrium, is associated with fertility impairment, yet the contributions of the uterine immune microenvironment and molecular pathways are poorly understood. We hypothesized that adenomyosis disrupts fertility through impaired endometrial receptivity and immune dysregulation and explored the sphingosine-1-phosphate (S1P) pathway as a potential therapeutic target. 

Using a murine model of adenomyosis, we first confirmed a significant reduction in fertility and disruptions in estrous cyclicity. We then characterized the uterine immune microenvironment, revealing alterations in immune cell populations and inflammatory mediators. In addition, we observed defects in endometrial receptivity, including decreased HoxA10 expression and progesterone resistance. Finally, analysis of the S1P pathway and pharmacological inhibition showed a reduction of adenomyotic lesions, the extent of which depended on the timing of intervention. 

Overall, these findings establish a mechanistic link between adenomyosis, fertility impairment, and immune dysregulation, highlighting the S1P pathway as a promising therapeutic target and providing a foundation for future interventions aimed at improving reproductive outcomes in affected women.