Table 3.
The behaviors of CCL2 in different pregnancy outcomes at specific trimesters .
| Normal pregnancy | Abortion | Pre-eclampsia | Preterm labor |
|---|---|---|---|
| Attracts macrophages to keep a balanced immune state in the first trimester (34) | Recruits more M1 macrophages to secret more pro-inflammatory factors in the early trimester (125, 126) | Enhances Fas-intermediated apoptosis of EVT in the second trimester (137) | Increases the infiltration of neutrophils and impairs immune tolerance in the last trimester (142, 143) |
| Recruits Th17 for generating IL-17 to endorse trophoblast proliferation and control the apoptosis in the first trimester (32) | Mediates the alteration of T cells to Th1 and the generation of Th1 cytokines, leading to immune variations in the first trimester (86, 124) | Accumulates excess ROS to disturb the proliferation of trophoblasts in the second trimester (134) | |
| Produces the bias of Th2 polarization for the toleration of gestation in the first trimester (35, 40) | Attracts circulating monocytes to damage the vascular endothelium in the second trimester (137) | ||
| Enhances the proliferation and vigor of ESC through Akt and MAPK/Erk1/2 signaling pathway, for decidualization in the first trimester (93, 94, 97) | Leads to systematic inflammatory disorders in the third trimester (140) | ||
| Regulates the growth and invasion of EVT for deeper implantation in the first trimester (98) | |||
| Prompts the proliferation and anti-apoptosis of DSC in the first trimester (51, 52) | |||
| Rationalizes the M1/M2 ratio for appropriate vascular transformation in the second trimester (109) | |||
| Increases the level of proangiogenic factors for vascular remodeling in the second trimester (114, 115) | |||
| Recruits more macrophages into uterine tissues for an “inflammatory microenvironment” in the last trimester and the onset of parturition (48) |