The role of IP-10 and its receptor CXCR3 in early pregnancy

The local immune microenvironment of the uterus plays an important role in a successful pregnancy. IP-10 (CXCL10) has been extensively studied in many immune-related diseases. However, the immune role of IP-10 in early pregnancy has not been fully recognized. This study mainly investigated the role of pro-inflammatory chemokine IP-10 in pregnancy. The levels of IP-10 and its receptor chemokine receptor 3 (CXCR3) were lower in the decidual tissues of an abortion-prone mice than in normal pregnant mice. Meantime, the expression of IP10 and CXCR3 was higher in the decidual tissues of early pregnant women than in the endometrial tissues of nonpregnant women. IP-10 promoted the production of interleukin 17 (IL-17) and interferon gamma (IFN-gamma), and also promoted the migration and differentiation of uterine decidual T cells to type 1 T helper (Th1) cells and Th17 cells. The abortion rate of early pregnant mice increased but the number of CD49b(+), CD11b(+), and CD3 epsilon(+) cells in the decidual tissues decreased upon treatment with anti-IP-10 antibody. Moreover, anti IP-10 antibody decreased the expression of RANTES but increased the expression of anti-inflammatory cytokines IL-6 and IL-10. A successful pregnancy requires the participation of IP-10. IP-10 participates in formation of the pro inflammatory immune microenvironment during early pregnancy by regulating the distribution of immune cells and promoting the production of pro-inflammatory cytokines.