Immune Cell Imbalance in Major Depressive and Panic Disorders

Marazziti, Donatella; Ambrogi, F; Vanacore, Renato; Mignani, V.; Savino, Mario; Palego, Lionella; Cassano, Giovanni B.; Akiskal, Hagop S.

doi:10.1159/000118891

Cited by 50 publications

(31 citation statements)

References 10 publications

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“…At present, the population of lymphocytes presenting 5HT transporter still has to be determined, but it is clear that a selective subtype of immune-circulating cells may have possible uptake sites for 5HT, but confi rmation in immune cells is lacking. CD3+ cells, which coexpress CD4+ and CD8+ antigens [38,39] , were counted and this group of depressed patients had a low number of positive CD3+ cells, in agreement with a previous study [40] . Further studies will be required to identify the distribution of these proteins on immune cells and the ensuing functional implications in health and disease.…”

Section: P42 C43 P44 P51 C52supporting

confidence: 88%

Allelic Isoforms and Decrease in Serotonin Transporter mRNA in Lymphocytes of Patients with Major Depression

Lima

Mata

Urbina

2005

Neuroimmunomodulation

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Serotonin transporter, measured by the specific binding of [³H]paroxetine, has been reported to be reduced in circulating lymphocytes of patients with major depression. Due to this observation, the objective of the present report was to determine the levels of serotonin transporter mRNA in lymphocytes obtained from 29 major depression patients (4 men, age 33.10 ± 1.63 years) and from 30 subjects included as a control group (4 men, age 37.54 ± 2.18 years) using RT-PCR. The patients were diagnosed according to the criteria of the American Psychiatric Association, and had a severity of depression of 32.68 ± 1.55 determined by the Hamilton Rating Scale for Depression. The DNA was submitted to polymerase chain reaction with primers for the 5′ regulatory region of human serotonin transporter, which could show the long and the short allelic forms of the transporter gene for the 5HTTLPR polymorphism. Semiquantitative analysis was performed using β-actin as internal and external standard. Control subjects presented the two allelic forms in 9.09% and depressed patients in 8.69%. The long variant was present in 73% of controls and in 60% of patients, without significant differences. There was a significant reduction in mRNA in depressed patients expressing the long allele. The number of immunofluorescent lymphocytes, labeled with a specific antibody against serotonin transporter, was reduced in the patients, as well as CD3+ lymphocytes. Serotonin and 5-hydroxyindoleacetic acid in platelet-poor plasma or lymphocytes did not differ between depressed patients and controls. The reduction in lymphocyte serotonin transporter described in major depression might be due to a decrease in the level of its mRNA and in the number of cells expressing it. These observations might implicate that functional modifications are associated with nervous-immune interactions in depression.

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Section: P42 C43 P44 P51 C52supporting

confidence: 88%

Allelic Isoforms and Decrease in Serotonin Transporter mRNA in Lymphocytes of Patients with Major Depression

Lima

Mata

Urbina

2005

Neuroimmunomodulation

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“…The authors used the plaque-forming cell assay and performed basal measures only, which may explain the discongruency between their results and ours. In a number of studies in depression, changes in T cells, B cells, or T cell subsets have been reported, though the results are conflicting (Schleifer et al 1989: Marazziti et al 1992. Quantative changes in the distribution of these parameters could be an inherent feature in depression, irrespective of plasma cortisol levels.…”

Section: Discussionmentioning

confidence: 99%

Immunoglobulin production in vitro in major depression: A pilot study on the modulating action of endogenous cortisol

Kok

Heijnen

Bruijn

et al. 1995

Biological Psychiatry

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“…Stimulation with anti-CD3+ induced significantly lower expression of CD25+ in generalized anxiety disorder patients when compared to controls [4]. In addition, patients with panic disorder had significantly lower CD4+ levels than healthy controls and depressive disorder patients [5]. In contrast, panic disorder patients had significantly higher levels of T4 [6, 7], natural killer cells, CD19 cells (B lymphocytes), human leukocyte antigen-DR-presenting cells [8], serum immunoglobulin A (IgA) [7]and interleukin (IL)-2 [9]than normal controls.…”

Section: Introductionmentioning

confidence: 99%

Reduced Anxiety Level by Therapeutic Interventions and Cell-Mediated Immunity in Panic Disorder Patients

Koh

Lee

2004

Psychother Psychosom

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Objective: This study examined the relationship between reduced anxiety level by therapeutic interventions and cell-mediated immunity (CMI) in patients with panic disorder. Methods: The subjects consisted of 42 patients with panic disorder and 42 normal gender- and age-matched controls. Among the patients, 21 were randomly assigned to a combined treatment of cognitive-behavioral therapy and the benzodiazepine antianxiety agent ethyl loflazepate (2 mg daily), and 21 were assigned to the antianxiety agent only. The treatment lasted for 6 weeks. Cell-mediated immune function was measured by the lymphocyte proliferative response to phytohemagglutinin (PHA) and interleukin-2 (IL-2) production. The anxiety level was assessed by the Hamilton Rating Scale for Anxiety and the anxiety subscale of the Symptom Checklist-90 Revised. Results: Prior to treatment, the panic disorder patients had significantly lower IL-2 production and blastogenic response to PHA than the normal controls. However, no significant differences in CMI were found between the pretreatment and posttreatment period in either the patient group receiving medication only or the combined treatment group, though after treatment, patients were significantly less anxious than before treatment in both intervention groups. The delta change (posttreatment value minus pretreatment value) in the self-reported anxiety level was significantly associated with the delta change in the blastogenic response in the combined treatment group. Conclusion: These findings suggest that panic disorder may be associated with decreased CMI, and the reduced level of self-reported anxiety in the patients who underwent combined therapeutic intervention is likely to increase the blastogenic response. Further studies are needed to evaluate the long-term effects of treatment on immune function.

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Immune Cell Imbalance in Major Depressive and Panic Disorders

Cited by 50 publications

References 10 publications

Allelic Isoforms and Decrease in Serotonin Transporter mRNA in Lymphocytes of Patients with Major Depression

Allelic Isoforms and Decrease in Serotonin Transporter mRNA in Lymphocytes of Patients with Major Depression

Immunoglobulin production in vitro in major depression: A pilot study on the modulating action of endogenous cortisol

Reduced Anxiety Level by Therapeutic Interventions and Cell-Mediated Immunity in Panic Disorder Patients

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