Glucocorticoids and immune function: unknown dimensions and new frontiers

Wilckens, Thomas; Rijk, Roel de

doi:10.1016/s0167-5699(97)01111-0

Cited by 329 publications

(219 citation statements)

References 67 publications

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“…Findings would have been more compelling if cortisol, rather than dexamethasone, had been used to suppress the production of cytokines. Although both of these agents have anti-inflammatory properties, dexamethasone is nearly 30 times more potent and primarily operates through a different isoform of the glucocorticoid receptor (Wilckens & DeRijk, 1997). Future studies may resolve this problem, and enhance their chances of detecting subtle alterations in glucocorticoid sensitivity, by using a cortisol-based assay system.…”

Section: Discussionmentioning

confidence: 99%

Chronic psychological stress and the regulation of pro-inflammatory cytokines: A glucocorticoid-resistance model.

Miller¹,

Cohen²,

Ritchey³

2002

Health Psychology

779

647

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This study examined whether chronic stress impairs the immune system's capacity to respond to hormonal signals that terminate inflammation. Fifty healthy adults were studied; half were parents of cancer patients, and half were parents of healthy children. Parents of cancer patients reported more psychological distress than parents of healthy children. They also had flatter diurnal slopes of cortisol secretion, primarily because of reduced output during the morning hours. There was also evidence that chronic stress impaired the immune system's response to anti-inflammatory signals: The capacity of a synthetic glucocorticoid hormone to suppress in vitro production of the pro-inflammatory cytokine interleukin-6 was diminished among parents of cancer patients. Findings suggest a novel pathway by which chronic stress might alter the course of inflammatory disease.

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Section: Discussionmentioning

confidence: 99%

Chronic psychological stress and the regulation of pro-inflammatory cytokines: A glucocorticoid-resistance model.

Miller¹,

Cohen²,

Ritchey³

2002

Health Psychology

779

647

View full text Add to dashboard Cite

show abstract

“…Adrenal-derived glucocorticoids suppress innate and specific immune responses through their negative actions on the expression of inflammatory mediators such as cytokines and cytokine receptors (5,47,48). Although widely used clinically, they clearly have protean effects and are far from optimal immunosuppressive agents.…”

Section: Discussionmentioning

confidence: 99%

“…To date, however, there are no clear candidates for glucocorticoid-induced genes that cause cell death. Alternatively, glucocorticoids also have positive effects on immune development and function (5). The GR and the TCR independently induce apoptosis, yet together they promote T cell survival (9).…”

mentioning

confidence: 99%

Positive Effects of Glucocorticoids on T Cell Function by Up-Regulation of IL-7 Receptor α

Franchimont

Galon

Vacchio

et al. 2002

The Journal of Immunology

145

102

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Despite the effects of glucocorticoids on immune function, relatively little is known about glucocorticoid-inducible genes and how their products may regulate lymphocyte function. Using DNA microarray technology to analyze gene expression in PBMC from healthy donors, we identified IL-7Rα as a glucocorticoid-inducible gene. This observation was confirmed at the mRNA and protein levels. Conversely, TCR signaling decreased IL-7Rα expression, and the relative strength of signaling between these two receptors determined the final IL-7Rα levels. The up-regulation of IL-7Rα by glucocorticoids was associated with enhanced IL-7-mediated signaling and function. Moreover, IL-7-mediated inhibition of apoptosis at increasing concentrations of glucocorticoids is consistent with enhanced cell sensitivity to IL-7 following glucocorticoid exposure. These observations provide a mechanism by which glucocorticoids may have a positive influence on T cell survival and function.

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“…24,36]. Since as early as 1949, glucocorticoids have been used to inhibit overt inflammatory responses, such as arthritis and colitis [37].…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids protect against suppression of T cell responses in a murine model of acute ethanol exposure and thermal injury by regulating IL-6

Faunce

Gregory

Kovacs

1998

Journal of Leukocyte Biology

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Previous reports by this laboratory demonstrated that acute alcohol exposure combined with a 15% body surface area dorsal scald injury results in significant reductions in delayed-type hypersensitivity (DTH) and splenocyte proliferative responses compared to either insult alone. Previous studies by this lab have also shown that these defects are mediated, in part, by increased production of interleukin-6 (IL-6). Because both alcohol exposure and thermal injury are known to modulate glucocorticoid (CORT) levels, and CORT regulates IL-6 gene expression, the relationship between circulating CORT and IL-6 production in burn ؉ ethanol mice was examined . At 24 and 48 h post-burn, a positive correlation existed between circulating CORT levels and measurements of cellular immune function. Administration of exogenous CORT to burn ؉ ethanol-treated mice resulted in significant restoration (to 60% of control) of DTH and splenocyte proliferative responses. This restoration was concomitant with a down-regulation of circulating and macrophage-derived IL-6. The specificity of CORT in modulating these responses was tested by assessing cellular immune function and IL-6 levels after glucocorticoid receptor blockade with RU486. Taken together, these data strongly suggest that under normal circumstances CORT protects burned mice from severe immune dysfunction, a protection that is not afforded to burn ؉ ethanol-treated mice. Furthermore, the immune dysfunction observed in burn ؉ ethanol mice may be due to a lack of glucocorticoid attenuation of IL-6. J. Leukoc. Biol. 64: 724-732; 1998.

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Glucocorticoids and immune function: unknown dimensions and new frontiers

Cited by 329 publications

References 67 publications

Chronic psychological stress and the regulation of pro-inflammatory cytokines: A glucocorticoid-resistance model.

Chronic psychological stress and the regulation of pro-inflammatory cytokines: A glucocorticoid-resistance model.

Positive Effects of Glucocorticoids on T Cell Function by Up-Regulation of IL-7 Receptor α

Glucocorticoids protect against suppression of T cell responses in a murine model of acute ethanol exposure and thermal injury by regulating IL-6

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