Immune disorders in depression: higher T helper/T suppressor‐cytotoxic cell ratio

Maes, Michaël; Stevens, W. J.; DeClerck, Luc; Bridts, Chris H.; Peeters, Dirk; Schotte, Christiaan; Cosyns, Paul

doi:10.1111/j.1600-0447.1992.tb03292.x

Cited by 85 publications

(47 citation statements)

References 44 publications

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“…As reported in most other PTSD studies, the psychological evaluations indicated that current or past depression was common in those with a history of maltreatment. While other papers have reported that that major depressive disorder can affect the CD4+CD45RA+ cell subset (Maes et al, 1992), the current results were not secondary to depressive symptoms. Moreover, the regression models indicated that intrusion even more than avoidance was related to the cell activation.…”

Section: Discussioncontrasting

confidence: 86%

“…This methodological issue is extremely important because many subclinical illnesses and psychological disorders can create a proinflammatory physiological state, which could drive the activation of lymphocytes (Maes et al, 1992). The issue of whether or not to include individuals with minor clinical conditions or using medications is a methodological challenge for any project of this type.…”

Section: Discussionmentioning

confidence: 99%

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Symptom severity predicts degree of T cell activation in adult women following childhood maltreatment

Lemieux

Coe

Carnes

2008

Brain, Behavior, and Immunity

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Although depression is often associated with a reduction in cellular immune responses, other types of emotional disturbance and psychopathology can activate certain aspects of immunity. Activation markers on T cells, in particular, have been found to be elevated in post-traumatic stress states. However, little is known about the relationship between the severity of PTSD symptoms and the degree of change in T cell phenotypes, or about the potential role of neuroendocrine factors in mediating the association. Twenty-four women with a history of sexual trauma during childhood, including 11 who met diagnostic criteria for PTSD, were compared to 12 age-matched, healthy women without a history of maltreatment. The women provided fasted blood samples for enumeration of cell subsets by immunofluorescence and 24-hour urine samples for analysis of catecholamine and cortisol levels. The percent of T cells expressing CD45RA, an early activation marker, was higher in the PTSD diagnosed women, and the levels correlated positively with intrusive symptoms and negatively with avoidant symptoms. These alterations in cell surface markers did not appear to be mediated by norepinephrine (NE) or cortisol, making them a distinctive and independent biomarker of arousal and disturbance in PTSD.

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Section: Discussioncontrasting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Symptom severity predicts degree of T cell activation in adult women following childhood maltreatment

Lemieux

Coe

Carnes

2008

Brain, Behavior, and Immunity

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“…Early studies showed an increase of T-helper cells (CD4 ' cells) and an increased CD4 ' /CD8 ' ratio in depressive disorders (Syvalähti et al 1985;Maes et al 1992;Mü ller et al 1993). Further investigations of the cellular components of the immune system focussed on monocytes and macrophages.…”

Section: Immune Cellsmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

227

126

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Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.

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“…Activation of the inflammatory response system in major depression (MD) is well documented [1,2,3,4,5]. Two recent meta-analyses clearly showed elevated interleukin (IL)-6 levels in patients with MD [6,7].…”

Section: Introductionmentioning

confidence: 99%

Immunology of Major Depression

Müller¹

2014

Neuroimmunomodulation

149

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High levels of several proinflammatory components of the immune system, such as interleukin-6, C-reactive protein, tumor necrosis factor (TNF)-α, or neopterin in patients suffering from major depression (MD) point to the involvement of an inflammatory process in the pathophysiology of MD. The direct and indirect effects of cytokines on neurotransmitter storage and release - mediated by microglia cells and astrocytes - are discussed. The tryptophan/kynurenine metabolism is one of the indirect mechanisms because the enzyme indoleamine 2,3-dioxygenase - a key enzyme of this metabolism in the central nervous system - is driven by pro- and anti-inflammatory cytokines and degrades serotonin. Moreover, neuroactive kynurenines such as kynurenic acid and quinolinic acid act on the glutamatergic neurotransmission as N-methyl-D-aspartate antagonists and agonists, respectively. Alterations of the serotonergic, noradrenergic and glutamatergic neurotransmission have been shown with low-level neuroinflammation and may be involved in symptom generation. Epidemiological and clinical studies show a role for inflammation as a risk factor for MD. A large-scale epidemiological study in MD clearly demonstrates that severe infections and autoimmune disorders are lifetime risk factors for MD. The vulnerability-stress-inflammation model matches with this view as stress may increase proinflammatory cytokines and even contribute to a lasting proinflammatory state. Further support comes from the therapeutic benefit of anti-inflammatory medications such as the cyclo-oxygenase-2 inhibitors, TNF-α antagonists and others, and the anti-inflammatory and immunomodulatory intrinsic effects of antidepressants.

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Immune disorders in depression: higher T helper/T suppressor‐cytotoxic cell ratio

Cited by 85 publications

References 44 publications

Symptom severity predicts degree of T cell activation in adult women following childhood maltreatment

Symptom severity predicts degree of T cell activation in adult women following childhood maltreatment

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Immunology of Major Depression

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