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Studies in mice have suggested that the placenta is protected from immune rejection by maternal T cells by means of localised indoleamine 2,3-dioxygenase dependent depletion of tryptophan. To determine whether such mechanisms might operate in the human placenta, we have studied the physiological importance of human placental indoleamine 2,3-dioxygenase immunohistochemically and functionally. Indoleamine 2,3-dioxygenase is detectable immunohistochemically from day 6 human blastocysts and thereafter throughout pregnancy in syncytiotrophoblasts, extravillous cytotrophoblasts and macrophages in the villous stroma and in the fetal membranes. Interferon-gamma added to villous explants markedly stimulates indoleamine 2,3-dioxygenase protein expression in macrophages. Indoleamine 2,3-dioxygenase-mediated tryptophan degradation in the first trimester villous and decidual tissue explants is stimulated by interferon-gamma and inhibited by 1-methyl-tryptophan (an inhibitor of indoleamine 2,3-dioxygenase). Peripheral blood mononuclear cell proliferation is controlled by indoleamine 2,3-dioxygenase-mediated tryptophan degradation. These results suggest the cellular basis of a mechanism present at the human maternal-fetal interface involved in regulating the maternal immune response to conceptus.

Original publication

DOI

10.1016/j.jri.2003.11.004

Type

Journal article

Journal

J Reprod Immunol

Publication Date

04/2004

Volume

61

Pages

87 - 98

Keywords

Antiviral Agents, Blastocyst, Cell Division, Culture Techniques, Extraembryonic Membranes, Female, Gene Expression Regulation, Developmental, Humans, Immunohistochemistry, Interferon-gamma, Leukocytes, Mononuclear, Lymphocyte Activation, Macrophages, Maternal-Fetal Exchange, Placenta, Pregnancy, T-Lymphocytes, Tryptophan, Tryptophan Oxygenase