Problem: The hypothesis that indoleamine 2,3-dioxygenase (IDO) is necessary to regulate lymphocyte functions at the feto-maternal interface has been postulated, although a possible role of tryptophan (Trp) depletion in the T-cell tolerance during insemination as well as implantation has not been previously investigated.
Method of study: Allogeneic phytohaemagglutinin stimulated lymphocytes were supplemented with pre-implantation embryo supernatant (PES), seminal plasma (SP), spermatozoa culture supernatant (SCS), spermatozoa, trophoblast cells, or placenta explant culture supernatants, and analyzed for expression of CD25, CD71, and CD69. Trp-degrading activity was assessed by addition of 1-methyl-Tryptophan or L-Trp.
Results: PES, SP, trophoblast, and explant supernatants reduced the expression of CD25 in CD3 lymphocytes. Inhibition of IDO as well as Trp supplementation prevented these effects.
Conclusions: These data suggest that the expression of interleukin-2 (IL-2) receptor in maternal T lymphocytes is normally suppressed by Trp catabolism, and that either abnormal IDO levels or substances influencing IDO activity might lead to non-adequate immune responses on sperm, harm the conceptus or even initiate fetal rejection.