Although two recent reports have demonstrated that exposure to TNF and IL1B increases MIF protein and mRNA levels in stromal cells derived from cycling human endometrium, the current results indicate that while MIF is synthesized and secreted at high concentrations by term decidual cells, its expression is not regulated by TNF or IL1B. Previous studies have demonstrated that MIF can induce, either directly or indirectly, the production of several proinflammatory molecules, including cytokines, nitric oxide, and prostaglandins.
The constitutive expression of MIF by decidual cells revealed in the present study is likely to modulate the delicate equilibrium between proinflammatory and anti-inflammatory factors, which is crucial for the maintenance of pregnancy. Thus, the absence of regulation of MIF production by decidual cells following TNF and IL1B exposure demonstrated in the current study could be an important previously undisclosed mechanism for preventing an exaggerated inflammatory response at the implantation site.
Decidual macrophages regulate trophoblast migration and proliferation, and are likely to play important roles in controlling the local maternal immune response as well as immunological rejection of the semi-allogenic embryo.