Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression.

By T. Pace, Fang Hu, Andrew H. Miller. Brain, behavior, and immunity, 2007

618 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Endocrinology, Diabetes and Metabolism

View Paper: https://www.semanticscholar.org/paper/f17153832a4d27bb7df70366f7783b7b052939da

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In Behavioral Neuroscience

In Endocrinology, Diabetes and Metabolism

Citations in the corpus

Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression (2009, neutral): “Cytokines can also influence GR expression, leading to decreased GR alpha, the active form of the receptor, and increased GR beta, a relatively inert GR isoform (57).”
Psychological Stress in Childhood and Susceptibility to the Chronic Diseases of Aging: Moving Towards a Model of Behavioral and Biological Mechanisms (2011, background): “For example, cytokine exposure can induce phosphorylation of some GR residues in white blood cells (Pace et al., 2007).”
From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression (2014, background): “…in diurnal cortisol slope in depressed individuals may be explained by their levels of glucocorticoid sensitivity (Jarcho, Slavich, Tylova-Stein, Wolkowitz, & Burke, 2013; see also Anacker, Zunszain, Carvalho, & Pariante, 2011; Fries, Hesse, Hellhammer, & Hellhammer, 2005; Pace et al., 2007, 2011).”
ELEVATED INFLAMMATION LEVELS IN DEPRESSED ADULTS WITH A HISTORY OF CHILDHOOD MALTREATMENT (2008, neutral): “On the other hand, inflammation reduces glucocorticoid signaling, and reduced glucocorticoid signaling may lead to abnormal brain functioning.(9) Depressed individuals often have impaired glucocorticoid signaling(10) and may, therefore, be at higher risk of inflammation.”
Inflammatory Cytokines in Depression: Neurobiological Mechanisms and Therapeutic Implications (2013, background): “Therefore, it is reasonable that HPA-mediated vulnerability to cytokine-induced depression represents a more general hyper-responsiveness and preexisting vulnerability to stress or inflammatory challenge, which may be mediated by changes in glucocorticoid receptor (GR) expression or function (Pace e”
Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling (2009, background): “For example, the GR can be phosphorylated by MAP kinases, which desensitizes it to cortisolmediated signaling and, in doing so, facilitates proinflammatory activity by NF- B (24).”
Inflammation: depression fans the flames and feasts on the heat. (2015, background): “Inflammatory overresponsiveness maysteminpart fromdecreasedglucocorticoidstressresponses (26, 154, 195), and blunted glucocorticoid signaling in concert with increased NF-kB signaling may provide one functional fingerprint for chronic stress (154).”
Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, background): “…Neuropsychopharmacology REVIEWS domain (that is unable to bind to known glucocorticoids) and a unique pattern of gene regulation (Pace et al, 2007; Kino et al, 2009).”
The Neuroendocrinology of Social Isolation (2014, background): “…the glucocorticoid receptor becomes less efficient in transducing endogenous glucocorticoid signals (e.g., Cole et al. 2009, Hanke et al. 2012, Pace et al. 2007, Powell et al. 2013), thereby increasing an inflammatory biology that can contribute to the development of diseases ranging from…”
Depressive disorders and immunity: 20 years of progress and discovery. (2007, background): “…to potently inhibit inflammatory signaling pathways, pharmacologic agents that enhance glucocorticoid signaling and/or inhibit inflammatory signaling, including type 4 phospodiesterase inhibitors, may be worthy of consideration (McKay and Cidlowski, 1999; Miller et al., 2002a; Pace et al., 2007).”
Social regulation of gene expression in human leukocytes (2007, background): “This hypothesis is consistent with previous indications of receptor-mediated glucocorticoid insensitivity during behavioral stress [38,40], and with recently identified molecular mechanisms of GR transcriptional inhibition [37].”
Cytokines and their relationship to the symptoms and outcome of cancer (2008, background): “In people with depression there is evidence of malfunction of cortisol receptors leading to cytokine-induced cortisol resistance, impaired feedback inhibition of the HPA axis and sustained activation of immune cell”
Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017, background): “Finally, cytokines can impair GR function by disrupting GR translocation and inhibiting downstream GR signaling, including NFκB and mitogen-activated protein kinase cascades (Miller et al, 1999; Pace et al, 2007).”
From inflammation to sickness and depression: when the immune system subjugates the brain (2008, background): “In addition, pro-inflammatory cytokines seem to promote expression of the β isoform of the glucocorticoid receptor that is inactive but still able to bind its ligan”