Syvälahti E, Eskola J, Ruuskanen O, Laine T
Prog Neuropsychopharmacol Biol Psychiatry. 1985;9(4):413-22. doi: 10.1016/0278-5846(85)90195-2.
Eighteen depressive patients and twenty-five healthy control subjects were studied using a comprehensive immunological test system and the dexamethasone suppression test (DST) as well as some additional neuroendocrine parameters. In addition, immune functions of six of the patients were studied serially three times at 1-2 month's intervals. The OKT 4+/8+ ratio (OKT 4+ = helper/inducer phenotype; OKT 8+ = suppressor/cytotoxic phenotype) was slightly higher in those ten depressive patients showing suppression in the DST than in healthy controls, but there were no significant differences between the nonsuppressor and suppressor groups or between the nonsuppressor and suppressor groups or between nonsuppressors and control subjects. Lymphocyte transformation responses induced by phytohaemagglutinin (PHA) were similar in the nonsuppressors and suppressors, but lower in both groups than in control subjects. The number of Ig-secreting cells measured in the absence and presence of pokeweed mitogen (PWM) were similar in the nonsuppressor and suppressor groups. Four of the depressive patients tested repeatedly exhibited an abnormal response in the DST at the beginning of the study. During the follow-up period two of them recovered completely from depression as well as the patients with a normal suppression in the DST. The proportions of T and B lymphocytes and regulatory T lymphocyte subsets as well as the functions of T and B lymphocytes of the nonsuppressors and suppressors in the DST were within normal ranges before and after recovery from depression and comparable to healthy controls in repeated testing. The results indicate that in spite of the importance of cortisol in immunoregulation, the increased cortisol secretion and typical resistance to dexamethasone suppression in endogenously depressive patients is not profoundly and consistently reflected in immune functions. Neither does normalization of cortisol responses induce any major changes in immune status during a patient's recovery from depression. Previous work indicates that suppressed immunity may play an important role in the increased morbidity and mortality associated with bereavement. In the light of present findings we suggest that endogenous depression differs also in this respect from grief reactions.
使用综合免疫测试系统、地塞米松抑制试验（DST）以及一些其他神经内分泌参数，对18名抑郁症患者和25名健康对照者进行了研究。此外，对其中6名患者的免疫功能每隔1 - 2个月进行了3次连续研究。在DST中表现出抑制的10名抑郁症患者的OKT 4 + / 8 + 比值（OKT 4 + =辅助/诱导表型；OKT 8 + =抑制/细胞毒性表型）略高于健康对照者，但非抑制组与抑制组之间或非抑制组与健康对照者之间无显著差异。植物血凝素（PHA）诱导的淋巴细胞转化反应在非抑制组和抑制组中相似，但两组均低于对照者。在有无商陆有丝分裂原（PWM）情况下测得的分泌免疫球蛋白细胞数量在非抑制组和抑制组中相似。在研究开始时，接受重复测试的4名抑郁症患者在DST中表现出异常反应。在随访期间，其中2名患者从抑郁症中完全康复，DST中抑制正常的患者也是如此。非抑制组和抑制组中T和B淋巴细胞以及调节性T淋巴细胞亚群的比例以及T和B淋巴细胞的功能在抑郁症康复前后均在正常范围内，并且在重复测试中与健康对照者相当。结果表明，尽管皮质醇在免疫调节中很重要，但内源性抑郁症患者皮质醇分泌增加和对地塞米松抑制的典型抵抗在免疫功能中并未得到深刻而持续的体现。在患者从抑郁症中康复期间，皮质醇反应的正常化也不会引起免疫状态的任何重大变化。先前的研究表明，免疫抑制可能在与丧亲相关的发病率和死亡率增加中起重要作用。根据目前的研究结果，我们认为内源性抑郁症在这方面也与悲伤反应不同。
