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Comparative Effects of l ‐Tryptophan and 1‐Methyl‐Tryptophan on Immunoregulation Induced by Sperm, Human Pre‐implantation Embryo and Trophoblast Supernatants
Author(s) -
Gutiérrez G.,
Fitzgerald J. S.,
Pöhlmann T.,
Hoppe I.,
Markert U. R.
Publication year - 2003
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1572-0241.2004.40012.x-i1
Subject(s) - trophoblast , biology , il 2 receptor , conceptus , embryo , andrology , immune system , endocrinology , placenta , medicine , immunology , t cell , microbiology and biotechnology , fetus , pregnancy , genetics
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.