Impaired lymphocyte function in depressive illness

Kronfol, Ziad; Silva, Joseph; Greden, John F.; Dembinski, Susan; Gardner, Robert; Carroll, Bernard J.

doi:10.1016/0024-3205(83)90382-x

Cited by 277 publications

(78 citation statements)

References 15 publications

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“…The higher DPM following PWM stimulation in depressed patients did not reach even trend level. Our results differ from several observations reporting a clear-cut attenuated mitogen response following administration of various lectins in depressed patients (Kronfol et al 1983;Schleifer et al 1984;Cosyns et al 1989). However, the mitogen-induced blastogenesis has recently been attributed more to factors such as age, severity of depression, and hospitalization effects than to the diagnosis itself (Schleifer et al 1989).…”

Section: Discussioncontrasting

confidence: 99%

“…A variety of studies have investigated lymphocyte subsets (Schleifer et al 1989), natural killer cell activity (Irwin et al 1988;Schleifer et al 1989), and the mitogen response to various lectins (Kronfol et al 1983;Schleifer et al 1984Schleifer et al , 1985Cosyns et al 1989). Although initial studies reported a decreased mitogen-induced leucocyte proliferation in depressed patients (Kronfol et al 1983;Schleifer et al 1984), this could not be consistently reproduced in later investigations (Schleifer et al 1985). Instead, other variables, such as age and severity of depression, seemed to play a key role for the lectin-induced blastogenesis (Schleifer et al 1989).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

In vivo and in vitro effects of glucocorticoids on lymphocyte proliferation in depression

Rupprecht

Wodarz

Kornhuber

et al. 1991

Eur Arch Psychiatry Clin Nuerosci

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European "D~I rg'~'~ Ir t"l~'I r Archives of 1~ y Ik.lllOl.lkl. Summary. Twelve severely depressed patients and 13 healthy controls were studied under baseline, metyrapone and metyrapone plus dexamethasone pretreated conditions. Lymphocyte proliferation data were obtained by concanavalin A, phytohaemagglutinin and pokeweed mitogen (PWM) stimulation. There was a decrease in PWM-induced B-cell proliferation and an increase in inhibition of spontaneous leucocyte proliferation by dexamethasone added in vitro following metyrapone administration in vivo, in healthy controls, which was not present in the depressed patients. These data support the concept of a decreased functional plasticity of the glucocorticoid receptor in depression also at the cellular level.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

In vivo and in vitro effects of glucocorticoids on lymphocyte proliferation in depression

Rupprecht

Wodarz

Kornhuber

et al. 1991

Eur Arch Psychiatry Clin Nuerosci

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“…Even though the studies reported in the five years prior to the 1989 report by Schleifer et al were based on small samples, the majority found significant decreases in mitogen-stimulated lymphocyte responses in unmedicated depressed patients as compared with control subjects (Kronfol et al 1983(Kronfol et al , 1986Schleifer et al 1984;Syvalahti et al 1985;Calabrese et al 1986;Darko et al 1988). Differences have been more distinct in studies of older patients and those hospitalized for more severe depressive disorders, suggesting either that age and/or severity of depression are independent determinants of impaired immunity or that a higher-order CNS disturbance is a cause of both the endogenous sub-type and immune dysfunction.…”

Section: Immune Dysfunction In Depressive Disordermentioning

confidence: 96%

Is there immune dysfunction in depressive disorders?

Hickie¹,

Silove²,

Hickie³

et al. 1990

Psychol. Med.

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“…211 Dysregulated activity of the immune system in depression, with increased proinflammatory activity, has repeatedly been demonstrated. [212][213][214][215][216] In addition, inflammatory diseases are typically associated with depressed mood. 217,218 Administration of proinflammatory cytokines (e.g.…”

Section: Stressmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

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Impaired lymphocyte function in depressive illness

Cited by 277 publications

References 15 publications

In vivo and in vitro effects of glucocorticoids on lymphocyte proliferation in depression

In vivo and in vitro effects of glucocorticoids on lymphocyte proliferation in depression

Is there immune dysfunction in depressive disorders?

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

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