Abstract
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 IP-10 and CXCR3 was higher in the decidual tissues of early pregnant women than in the endometrial tissues of non-pregnant women. IP-10 promoted the production of interleukin 17 (IL-17) and interferon gamma (IFN-γ), 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 CD3ε+ 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.