Objective: To examine the effect of unemployment on natural killer cell cytotoxicity (NKCC) and, in a subsample of persons who become re-employed, to determine if, after termination of the stressor, immune values recover to levels similar to matched controls.
Methods: One hundred unemployed and 100 matched employed healthy men and women, aged 29 to 45 years, were followed for 4 months with monthly blood samples taken to measure NKCC, the ability of NK cells to kill target cells. Twenty-five participants obtained employment before the end of the study, leaving 75 unemployed (and 75 employed) participants in the main sample. For unemployed participants who obtained employment before the end of the study, subsample analyses compared NKCC levels before and after obtaining a new job.
Results: The persistently unemployed sample had significantly lower NKCC levels for all three effector:target ratios (100:1, p = .0004; 50:1, p = .002; and 25:1, p = .02) when compared with the matched employed sample. There were no significant gender effects. In the subsample analyses, NKCC was significantly higher after the participants became employed, compared with their unemployed period, with substantial "recovery" of immune function (44%-72%) compared with values from the steadily employed group.
Conclusions: Chronic stress is associated with persistent NKCC impairment. When the chronic stressor is terminated, however, the immune cell functional capacity quickly begins to recover. We believe this is the first study in humans to document immune function recovery after the definable end of a chronic stressor.
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http://dx.doi.org/10.1097/PSY.0b013e31803139a6 | DOI Listing |
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Metabolic abnormalities associated with liver disease have a significant impact on the risk and prognosis of cholecystitis. However, the underlying mechanism remains to be elucidated. Here, we investigated this issue using Wilson's disease (WD) as a model, which is a genetic disorder characterized by impaired mitochondrial function and copper metabolism.
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Institute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Function-to-find domain (FIIND)-containing proteins, including NLRP1 and CARD8, are vital components of the inflammasome signaling pathway, critical for the innate immune response. These proteins exist in various forms due to autoproteolysis within the FIIND domain, resulting in full-length (FL), cleaved N-terminal (NT), and cleaved C-terminal (CT) peptides, which form autoinhibitory complexes in the steady state. However, the detailed mechanism remains elusive.
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