Galanaud P, Crevon M C, Emilie D, Abella A
Clin Immunol Immunopathol. 1983 Dec;29(3):403-14. doi: 10.1016/0090-1229(83)90043-0.
The specific plaque-forming cell response induced by trinitrophenyl polyacrylamide beads in cultures of nonadherent human peripheral blood mononuclear cells (PBM) is resistant to the inhibitory effect of hydrocortisone (HC). Previous results showed that low concentrations (up to 10(-7 M) of HC inhibit the same response in cultures of unfractionated human PBM. It is shown that the addition of 5-10% monocytes to nonadherent PBM renders their response HC-sensitive. One mechanism of the interaction between HC and monocytes is the potentiation of prostaglandin E2-mediated suppression by HC, which can be demonstrated in vitro and after in vivo administration of HC. However, interaction with a non-prostaglandin-mediated suppression by monocytes should be involved, particularly with high (10(-6) M) concentrations of HC.
三硝基苯基聚丙烯酰胺珠在非贴壁人外周血单个核细胞（PBM）培养物中诱导的特异性噬斑形成细胞反应对氢化可的松（HC）的抑制作用具有抗性。先前的结果表明，低浓度（高达10^(-7)M）的HC可抑制未分级人PBM培养物中的相同反应。结果表明，向非贴壁PBM中添加5-10%的单核细胞会使其反应对HC敏感。HC与单核细胞相互作用的一种机制是HC增强前列腺素E2介导的抑制作用，这在体外和体内给予HC后均可得到证实。然而，单核细胞介导的非前列腺素抑制作用也应参与其中，尤其是在高浓度（10^(-6)M）的HC作用下。
