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Inhibition of lnterleukin‐2 Production by Retroplacental Sera: A Possible Mechanism for Human Fetal Allograft Survival
Author(s) -
NICHOLAS N.S.,
PANAYI G.S.
Publication year - 1985
Publication title -
american journal of reproductive immunology and microbiology
Language(s) - English
Resource type - Journals
eISSN - 1600-0897
pISSN - 8755-8920
DOI - 10.1111/j.1600-0897.1985.tb00332.x
Subject(s) - mechanism (biology) , fetus , production (economics) , chemistry , microbiology and biotechnology , biology , andrology , immunology , pregnancy , medicine , genetics , philosophy , economics , microeconomics , epistemology
Fetal tolerance may be a consequence of a local nonspecific serum factor(s) having immunomodulatory activity on maternal cellular effector responses. Paired peripheral and retroplacental sera were collected from 15 healthy patients having elective caesarean section and the sera were studied for their abilities to inhibit the uptake of tritiated thymidine by activated lymphocytes in the mixed lymphocyte reaction (MLR). We found that:1) Twenty‐eight percent of peripheral blood (PB) and all retroplacental sera (RP) could inhibit the MLR. 2) Conditioned medium (MLRS) could completely overcome the inhibition by RP sera. 3) Ultrapure interleukin‐1 (IL‐1) could not reverse the inhibitory effect. 4) Recombinant interleukin‐2 (IL‐2) (100 units/culture) completely reversed the inhibition. 5) Inhibition by RP sera occurred between 0 and 24 hours of cell‐cell interactions in the MLR and, 6) The inhibition was both on stimulator and responder cells.Thus, factor(s) in RP sera may act to inhibit IL‐2 production at the fetomaternal interface. These findings are discussed in the context of fetal allograft rejection.