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Actions of Steroids and Prostaglandins Secreted by the Placenta and Uterus of the Cow and Ewe on Lymphocyte Proliferation In Vitro
Author(s) -
LOW B.G.,
HANSEN P.J.
Publication year - 1988
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.1600-0897.1988.tb00238.x
Subject(s) - conceptus , placenta , endocrinology , medicine , lymphocyte , in vitro , prostaglandin , biology , fetus , uterus , prostaglandin e , chemistry , pregnancy , biochemistry , genetics
Prostaglandins, steroids, and their metabolites that are known to be produced by the conceptus, maternal endometrium, and placenta of the cow and sheep were tested for their ability to inhibit in vitro blastogenesis of bovine and ovine lymphocytes. Prostaglandin E 2 (PGE 2 ) suppressed PHA‐ and mixed lymphocyte reaction‐induced blastogenesis in a log‐linear, concentration‐dependent manner, exerting its inhibitory effect at a final concentration of 10 −8 M and higher. PGE 2 also inhibited IL‐2 ‐dependent proliferation of lymphocytes, but to a lesser degree than for PHA‐treated cultures. Progesterone and estradiol‐17β also inhibited [ 3 H] thymidine incorporation into PHA‐stim‐ulated lymphocytes, but only at a pharmacological concentration of 10 −5 M. No synergy between PGE 2 and progesterone in inhibiting lymphocyte proliferation was observed. Estrone, PGF 2α , 15‐keto‐13,14‐dihydro‐PGF 2α , and two metabolites of progesterone (5β‐preg‐nane‐3,20‐dione and 5β‐pregnane‐3,20‐diol) had no effect on lymphocyte proliferation. By virtue of its continual production at the fetal‐maternal interface throughout pregnancy, PGE 2 may be an important local immunoregulatory agent to protect the allogeneic fetus from maternal immunological attack in the cow and ewe.