In the endometrium, IFN-т has been shown to stimulate granulocyte chemotactic protein-2 and monocyte che-motactic protein-1 and -2, IFN-7-inducible protein 10 kDa, IFN-stimulated gene product 17, 2’5′-oli-goadenylate-synthetase, 1-8U and Leu-13, major histocompatibility complex class I and beta-2-microglobu-lin, Mx protein, signal transducer and activator of transcription 1 and 2, interferon regulatory factor (IRF) 1 and IRF9. In the ovine uterus, the receptor for type I interferons is predominantly expressed in the luminal epithelium (LE) and shallow glands (SG) but also in the caruncular stroma. However, binding of IFN-т is limited to the LE and SG.
In immune cells, IFN-т stimulates the expression of interleukin (IL)-4, IFN-7, IL-2, and IL-10. It is also active in vivo across species, preventing fetal resorptions and experimental allergic encephalomyelitis in the mouse.
Additionally, IFN-т has been shown to regulate PG synthesis in endometrial cells in vitro, even though reports are contradictory because the responses appear to depend upon cell system and dose. At low doses, IFN-т inhibits the expression of cyclooxygenase (COX)-2 and the synthesis of PGs in endometrial epithelial and stromal cells, whereas at high doses it is stimulatory. Thus, IFN-т would either suppress the expression of COX-2 and the production of luteolytic PGF2a or induce COX-2 and the synthesis of luteoprotective/luteotropic PGE2.