Paternally derived antigens during allogenic pregnancy are expected to cause serious immunogenic problems without mechanisms that normally neutralize the maternal immune system. Local and systemic suppressor mechanisms are believed to work together to modulate the maternal immune responses while keeping the maternal ability to fight infections. The PD-L1 (the inhibitory ligand of PD-1), Galectin-9 (the inhibitory ligand of TIM-3), and Indoleamine-2, 3-dioxygenase 1 (IDO1) are among the interfering molecules for immunosuppression during pregnancy. Indoleamine-2, 3-dioxygenase (IDO) works during tryptophan catabolism to change it to kynurenine. Depletion of tryptophan serves as a mechanism for T cell-associated immune responses. Many studies have shown that IDO1 is expressed in the tissues in the maternal-fetal interface, especially trophoblast cells, decidual stroma cells, and decidual immune cells. Mesenchymal stem cells have been well documented for their immune-regulatory potentials, making them proper candidates for clinical application in immune-related diseases, and IDO1 plays a crucial role in elevating the regulatory capacity of these cells. We have established a biological model for higher expression of the IDO1 gene and confirmed this gene as a proper candidate for the management of immune-related complications .

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