Lomnitzer R, Phillips R, Rabson A R
Clin Immunol Immunopathol. 1983 Jun;27(3):378-86. doi: 10.1016/0090-1229(83)90090-9.
Hydrocortisone (HC) in pharmacologically attainable concentrations was shown to inhibit mitogen-induced lymphocyte blastogenesis. When adherent and nonadherent cells were treated separately with hydrocortisone and then reconstituted, treatment of either cell population resulted in a diminished mitogen-activated response. HC-treated adherent cells produced less interleukin 1 (IL-1) than control cells, and interleukin 2 (IL-2) production by HC-treated lymphocytes was also reduced. This latter finding could not be reversed by adding IL-1-containing adherent cell supernatants to the culture systems. Leukocyte inhibiting factor (LIF) production by sodium periodate-activated mononuclear cells was also reduced after HC treatment, but could be corrected by adding IL-1-containing adherent cell supernatants to the cultures. PHA-induced LIF production, which is less dependent upon adherent cells and their products, was not affected by HC treatment. It is concluded that HC exerts its suppressive effect by independently inhibiting IL-1 production by adherent cells and IL-2 production by lymphocytes.
药理学可达到浓度的氢化可的松(HC)被证明可抑制丝裂原诱导的淋巴细胞增殖。当贴壁细胞和非贴壁细胞分别用氢化可的松处理然后重新组合时,任一细胞群体的处理都会导致丝裂原激活反应减弱。经HC处理的贴壁细胞产生的白细胞介素1(IL-1)比对照细胞少,经HC处理的淋巴细胞产生的白细胞介素2(IL-2)也减少。通过向培养系统中添加含IL-1的贴壁细胞上清液,后一发现无法逆转。经HC处理后,高碘酸钠激活的单核细胞产生的白细胞抑制因子(LIF)也减少,但通过向培养物中添加含IL-1的贴壁细胞上清液可得到纠正。PHA诱导的LIF产生对贴壁细胞及其产物的依赖性较小,不受HC处理的影响。结论是,HC通过独立抑制贴壁细胞产生IL-1和淋巴细胞产生IL-2发挥其抑制作用。