The IL-23/Th17 axis in the pathophysiology of endometriosis

Studies have suggested the involvement of Th17 cell deregulation in endometriosis, in relation to disease severity. In this study, investigators examined whether IL-23-induced TH17 cells contribute to features of lesion proliferation, vascularization and inflammation in endometriosis using patient samples, representative cell lines and a mouse model of endometriosis. The data reveal deregulation of expression of key genes of the IL-23/Th17 axis in tissue samples and increased IL-23 secretion in the plasma of patients with endometriosis. In the mouse model, treatment targeting IL-23 altered the nature and progression of endometriosis lesions.