“…For the maternal immune system to prevent rejection of embryonic semiallograft, IFNT enhances the immune mechanisms at the maternal‐fetal interface by recruitment of monocytes to the endometrium or by regulating differentiation of the endometrium into macrophages or dendritic cells, with high levels of IFN‐induced genes, such as CCL2, CCL8, IL12B, pentraxin 3 (PTX3), radical S‐adenosyl methionine domain containing 2 (RSAD2), and tumor necrosis factor α (TNFA) in the bovine endometrium (Fair, ; Mansouri‐Attia et al, ). In addition, CCL2 is one of the most potent chemoattractants for immune regulatory cells, including monocytes, macrophages, T cells, and uNK cells in the endometrium, and plays a role in uterine cell proliferation, angiogenesis, and remodeling (Jones, Kelly, & Critchley, ; Salamonsen & Lathbury, ).…”