Wakasugi N, Virelizier J L
J Immunol. 1985 Jan;134(1):167-71.
Cord blood leukocytes (CBL) stimulated with PHA, Con A, or with the monoclonal antibody OKT3 proliferate normally but produce very low titers of IFN-gamma. This defect was not observed with maternal leukocytes collected at the time of delivery, indicating that the defective production of IFN-gamma in CBL is not a mere consequence of a hormonal change associated with labor. CBL produced large amounts of IFN-gamma (comparable to those observed in adult control and in mothers) after stimulation with staphylococcal enterotoxin A (SEA). Furthermore, gamma-irradiation with as little as 500 or 1000 rad, or incubation at 37 degrees C for 24 hr, reversed the defect in PHA-induced IFN-gamma secretion. This finding indicates that the defective secretion of IFN-gamma of CBL is not intrinsic, but rather is the consequence of a subtle dysregulation. We could not find evidence for a defective accessory function with cord blood monocytes, because the addition of adherent cells from adult donors did not reverse the defect. In co-cultures of adult leukocytes and CBL, PHA-induced IFN-gamma secretion was comparable to that of adult cultures tested alone. Nonirradiated CBL were not able to suppress IFN-gamma secretion by irradiated autologous leukocytes. Together, our results suggest that the defective PHA-induced IFN-gamma secretion of CBL is the result of an original type of dysregulation and is associated with an excessive sensitivity to suppressive signals rather than excessive suppressor function.
用PHA、Con A或单克隆抗体OKT3刺激的脐血白细胞（CBL）正常增殖，但产生的γ-干扰素滴度非常低。在分娩时采集的母体白细胞中未观察到这种缺陷，这表明CBL中γ-干扰素产生缺陷并非仅仅是与分娩相关的激素变化的结果。在用葡萄球菌肠毒素A（SEA）刺激后，CBL产生了大量的γ-干扰素（与在成年对照和母亲中观察到的相当）。此外，仅500或1000拉德的γ射线照射，或在37℃孵育24小时，可逆转PHA诱导的γ-干扰素分泌缺陷。这一发现表明，CBL的γ-干扰素分泌缺陷并非内在的，而是细微失调的结果。我们未发现脐血单核细胞辅助功能缺陷的证据，因为添加成年供体的贴壁细胞并不能逆转缺陷。在成年白细胞与CBL的共培养中，PHA诱导的γ-干扰素分泌与单独测试的成年培养物相当。未照射的CBL无法抑制照射后的自体白细胞分泌γ-干扰素。总之，我们的结果表明，CBL中PHA诱导的γ-干扰素分泌缺陷是一种原始类型失调的结果，并且与对抑制信号的过度敏感而非过度抑制功能相关。
