Inflammation influences progestins targets of endometrial cells refluxed in ectopic sites.
Inflammatory cytokines, like TNFα and IL-1β, can reduce the expression of progesterone receptors.
The same cytokines can increase the expression of glucocorticoid receptors.
These findings could contribute to the progesterone resistance observed in endometriosis.
This findings may suggest the design of more targeted therapies with an effective local activity.