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  • Title: Nonsuppression of cortisol in depression and immune function.
    Author: Syvälahti E, Eskola J, Ruuskanen O, Laine T.
    Journal: Prog Neuropsychopharmacol Biol Psychiatry; 1985; 9(4):413-22. PubMed ID: 4070644.
    Abstract:
    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.
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