Cell-surface expression of L-selectin (CD62L) by blood lymphocytes: Correlates with affective parameters and severity of panic disorder

Manfro, Gisele Gus; Pollack, Mark H.; Otto, Michael W.; Worthington, John J.; Rosenbaum, Jerrold F.; Scott, Laura-Louise; Kradin, Richard L.

doi:10.1002/(sici)1520-6394(2000)11:1<31::aid-da5>3.0.co;2-o

Cited by 18 publications

(17 citation statements)

References 51 publications

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“…Marazziti et al (7) reported significantly fewer Th cells and reduced Th/Ts ratios in panic disorder patients, and others have found increases (11, 12) or decreases (21) in B cell populations in panic disorder. However, our findings support a lack of a relation between this disorder and the absolute numbers of Th cells (9-12, 21), the B cells (7, 9), and NK cell (9, 10, 12, 21). …”

Section: Discussioncontrasting

confidence: 47%

Lymphocyte Subsets and Mood States in Panic Disorder Patients

et al. 2005

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This study was conducted to examine lymphocyte subset counts and mood states in panic disorder patients. Twenty patients with panic disorder and 20 age- and gender-matched normal healthy subjects were recruited for the study. We used the Spielberger State (STAIS) & Trait (STAIT) Anxiety Inventory, Hamilton Depression Rating scale (HAMD) and Hamilton Anxiety Rating scale (HAMA) to measure mood states in all subjects. Lymphocyte subsets counts were made by flow cytometry. Panic patients showed significantly higher scores for anxiety and depression than normal subjects. Panic patients showed no differences in terms of the numbers of immune cells, as compared with normal healthy subjects, other than a lower proportion of T suppressor cells and a higher T helper cell/T suppressor cell ratio. HAMA and STAIS scores were common factors that could predict T cell numbers and proportions, T helper cell numbers, and natural killer cell proportions in panic disorder patients. We suggest that anxiety levels are related to the T-cell population in panic disorder patients and that quantitative immune differences may reflect altered immunity in this disorder.

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Section: Discussioncontrasting

confidence: 47%

Lymphocyte Subsets and Mood States in Panic Disorder Patients

et al. 2005

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“…The importance of intrusion has also been highlighted in analyses on NK cell numbers and IL-2 receptor levels, where the influence was a suppressive one (Ironson et al, 1997); (La Via et al, 1996). A prior report on patients with panic disorder indicated they showed a trend for higher percentages of CD45RA+ cells, which was positively predicted by global severity of symptoms and, marginally, by anxious symptoms (Manfro et al, 2000). T cell numbers, in general, increase in the circulation immediately following an acute stressor, often due to increased sympathetic activity and changes in adhesion molecules that serve to release cells from the blood vessel wall (Mills et al, 1997).…”

Section: Discussionmentioning

confidence: 98%

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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“…Two studies examining immune function using circulating lymphocyte phenotypic markers in PD patients found evidence that individuals with PD may show alterations in circulating lymphocyte profiles or diminished cell activation (Manfro et al, 2000;Rapaport, 1998). Other evidence in a mixed anxiety disorder group found that those with anxiety disorders had lymphocyte and T-cell counts above the average range, as well as highly sensitized T-cell lymphocytes (Boscarino and Chang, 1999b).…”

Section: Fear-and Anxiety-based Disorders and Inflammationmentioning

confidence: 99%

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Michopoulos

Powers

Gillespie

et al. 2016

Neuropsychopharmacol

545

376

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The study of inflammation in fear-and anxiety-based disorders has gained interest as growing literature indicates that proinflammatory markers can directly modulate affective behavior. Indeed, heightened concentrations of inflammatory signals, including cytokines and C-reactive protein, have been described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.). However, not all reports indicate a positive association between inflammation and fear-and anxiety-based symptoms, suggesting that other factors are important in future assessments of inflammation's role in the maintenance of these disorders (ie, sex, co-morbid conditions, types of trauma exposure, and behavioral sources of inflammation). The most parsimonious explanation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the stress response and central and peripheral immune cells to release cytokines. Dysregulation of the stress axis in the face of increased sympathetic tone and decreased parasympathetic activity characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Taken together, the available data suggest that targeting inflammation may serve as a potential therapeutic target for treating these fear-and anxiety-based disorders in the future. However, the field must continue to characterize the specific role pro-inflammatory signaling in the maintenance of these unique psychiatric conditions.

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Cell-surface expression of L-selectin (CD62L) by blood lymphocytes: Correlates with affective parameters and severity of panic disorder

Cited by 18 publications

References 51 publications

Lymphocyte Subsets and Mood States in Panic Disorder Patients

Lymphocyte Subsets and Mood States in Panic Disorder Patients

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

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

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