Regular ArticleGlucocorticoid Regulation of Natural Cytotoxicity: Effects of Cortisol on the Phenotype and Function of a Cloned Human Natural Killer Cell Line☆
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2015, Pharmacology and TherapeuticsCitation Excerpt :Accordingly, treatment with inhaled corticosteroids (ICS) does not appear to reduce the levels of NKT cells in patients with asthma (Ikegami et al., 2004). In contrast, NK cells are highly susceptible to GC inhibition (Zhou et al., 1997). Glucocorticoid inhibition of NK activity is thought to involve calcium-dependent pathways (Gatti et al., 1987), and epigenetic modifications in the regulatory regions of pro-inflammatory genes (Eddy et al., 2014).
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2015, Brain, Behavior, and ImmunityCitation Excerpt :In this experiment, different mechanisms of action are represented through cortisol and PGE2. Cortisol was chosen due to its activation of a nuclear transcriptional mechanism (Zhou et al., 1997), whereas PGE2 activates an immediate cytoplasmatic cAMP-dependent mechanism (Torgersen et al., 1997). Epinephrine and PGs act through the same intracellular mechanism to suppress NKCC (Whalen and Bankhurst, 1990), but the effects of PGE2 were more potent at physiological levels than of epinephrine.
PGE<inf>2</inf> suppresses NK activity in vivo directly and through adrenal hormones: Effects that cannot be reflected by ex vivo assessment of NK cytotoxicity
2013, Brain, Behavior, and ImmunityCitation Excerpt :When removed before this assessment, no suppression was evident, and in PGE2- and epinephrine-ex-treated cells an increase in cytotoxicity (rebound) was observed. These findings correspond well with the known mechanism of enduring CORT action on NK cytotoxicity, mediated through activation of DNA-dependent mechanisms and protein synthesis (Zhou et al., 1997), in contrast to the transient cytoplasmatic-mediated effects of PGE2 and epinephrine in regulating NK activity, through elevation of cAMP and activation of PKA1 (Torgersen et al., 1997). Our herein in vitro findings also correspond with those of Hellstrand et al. (1985), reporting in vitro suppression of human NK activity by epinephrine, which was followed by a rebound effect following its removal.
Attachment style and immunity: A 1-year longitudinal study
2013, Biological PsychologyCitation Excerpt :These characteristics may be related to the finding of lower NKCC, as self-disclosure is associated with cellular immune function and health (Pennebaker et al., 1988), while increased stress and lower support in close relationships are correlated with poorer health and lower cellular immunity (Kiecolt-Glaser et al., 1993; Robles and Kiecolt-Glaser, 2003). Also, individuals high in attachment-related avoidance display altered hypothalamic–pituitary–adrenal axis reactivity to attachment-related stress tasks (Powers et al., 2006; Rifkin-Graboi, 2008), which may be relevant to the finding of reduced NKCC given the inhibitory effect of cortisol on NK cell-mediated lysis of target cells (Mavoungou et al., 2005; Zhou et al., 1997). Given that attachment style develops in childhood, is postulated to be related to the quality of interaction with the primary caregiver, and is characterized by substantial stability and continuity across the lifespan (Fraley, 2002; Grossmann et al., 2005; Mikulincer and Shaver, 2007), our findings may also be interpreted as consistent with the body of animal literature suggesting that early life factors such as quality of maternal care may have long-term effects on physiology (Coe, 1993; Liu et al., 1997).
COPD treatment: Real life and experimental effects on peripheral NK cells, their receptors expression and their IFN-γ secretion
2012, Pulmonary Pharmacology and TherapeuticsRole of sympathetic nervous system in the entrainment of circadian natural-killer cell function
2011, Brain, Behavior, and ImmunityCitation Excerpt :In other peripheral tissues, SCN lesions cause a loss of tissue NE rhythms and functionality (Cailotto et al., 2005; Terazono et al., 2003). It is likely the circadian regulation by rhythmic NE input from the SNS to the spleen acts in an integrative manner with other signals oscillating in a circadian rhythm, including glucocorticoids, prolactin, melatonin, and pro-opiomelanocortin-derived peptides (Boyadjieva et al., 2001; Currier et al., 2000; Gan et al., 2002; Sun et al., 2003; Zhou et al., 1997), to regulate the circadian expression and function of cytokines and cytolytic factors. Further studies would be necessary to determine how humoral signaling factors and neural inputs to the spleen and other peripheral tissues integrate timing information originating from the SCN.
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This work was supported in part by National Cancer Institute Grant CA 60823 (to D.M.C.) and the Research Excellence Program in Biotechnology, College of Arts & Sciences, Oakland University.
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Present address: Department of Biology, San Diego State University, San Diego, CA 92182-0057.
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To whom correspondence and reprint requests should be addressed at Department of Chemistry, Oakland University, Rochester, Michigan 48309.