Glucocorticoids and Immune Function

Munck, Allan; Guyre, Paul M.

doi:10.1016/b978-0-12-043780-1.50020-8

Cited by 165 publications

(93 citation statements)

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“…Their actions as anti-inflammatory and immunosuppressive drugs are both beneficial and detrimental. It is generally assumed that inhibition of the expression of proinflammatory cytokines such as IL-1a, IL-1b, IL-6, IL-8, TNF-a, IFN-a or IFN-b or induction of antiinflammatory cytokines such as IL-10 by GC underlies these effects [1,2]. Evidence is accumulating, however, that GC also have immunostimulatory properties, at least at physiological concentrations.…”

Section: Introductionmentioning

confidence: 99%

TCR signaling inhibits glucocorticoid-induced apoptosis in murine thymocytes depending on the stage of development

et al. 2005

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Section: Introductionmentioning

confidence: 99%

TCR signaling inhibits glucocorticoid-induced apoptosis in murine thymocytes depending on the stage of development

et al. 2005

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“…Specific pathogen-free female C57BL/6 mice, [8][9][10][11][12] wk old at the beginning of the experiments, were obtained from Charles River Labs. Specific pathogen-free C57BL/6J mice (referred to as wild-type [wt]), C57BL/6-ob mice (referred to as ob/ob ), and C57BL/Ks-db mice (further referred to as db/db )…”

Section: Methodsmentioning

confidence: 99%

“…This network is not only responsible for the deleterious outcome, but also for the induction of often more complex endogenous protection mechanisms whose function allows the organism to cope with the potentially autoaggressive consequences of immune/inflammatory reactions. Glucocorticoid hormones represent the most powerful antiinflammatory arm (8), whereas some proinflammatory cytokines, such as IL-1 and IL-6, play a dual role by also contributing to protective mechanisms via induction of acute-phase proteins (9). Some acute-phase proteins act as protease inhibitors to limit the destructive effects of TNF-induced proteases (10,11).…”

mentioning

confidence: 99%

Leptin Is an Endogenous Protective Protein against the Toxicity Exerted by Tumor Necrosis Factor

Takahashi

1999

Journal of Experimental Medicine

104

101

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SummaryTumor necrosis factor (TNF) is a central mediator of a number of important pathologies such as the systemic inflammatory response syndrome. Administration of high TNF doses induces acute anorexia, metabolic derangement, inflammation, and eventually shock and death. The in vivo effects of TNF are largely mediated by a complex network of TNF-induced cytokines and hormones acting together or antagonistically. Since TNF also induces leptin, a hormone secreted by adipocytes that modulates food intake and metabolism, we questioned the role of leptin in TNF-induced pathology. To address this question, we tested mouse strains that were defective either in leptin gene ( ob/ob ) or in functional leptin receptor gene ( db/db ), and made use of a receptor antagonist of leptin. Ob/ob and db/db mice, as well as normal mice treated with antagonist, exhibited increased sensitivity to the lethal effect of TNF. Exogenous leptin afforded protection to TNF in ob/ob mice, but failed to enhance the protective effect of endogenous leptin in normal mice. We conclude that leptin is involved in the protective mechanisms that allow an organism to cope with the potentially autoaggressive effects of its immune system.

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“…These permissive actions of glucocorticoids are in contrast to their well-known inhibitory effects on various immune and inflammatory responses. It is generally assumed that the inhibition of the production of cytokines by glucocorticoid hormones accounts for the suppressive effects of these hormones (26). However, a rather paradoxical picture emerges as glucocorticoids up-regulate the expression of cytokine receptors.…”

mentioning

confidence: 97%

Glucocorticoids Regulate TCR-Induced Elevation of CD4: Functional Implications

Wiegers

Stec

Klinkert

et al. 2000

The Journal of Immunology

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CD4 serves as a coreceptor during Ag recognition by the TCR. This interaction results in a marked increase in the sensitivity of a T cell to Ag presented by MHC class II molecules. Here we report that activation of T cells either by plate-bound mAb (anti-TCR, anti-CD3) or soluble activators (staphylococcal enterotoxin A, Con A) is associated with an (up to 3-fold) increase in CD4 cell surface expression on CD25+ cells, which was maximal after 72–96 h. Incubation with the glucocorticoid hormone corticosterone (CORT) shifted the enhancement of CD4 expression to a point about 24 h earlier than that observed in control cultures. In parallel, the proliferative response of these CORT-treated cells was profoundly enhanced. An involvement of increased CD4 expression in this enhanced proliferative response was evidenced by the observation that T cell proliferation in CORT-treated cultures was much less sensitive to inhibition by an inhibitory, nondepleting anti-CD4 mAb than that in control cultures. TCR down-regulation was, however, not affected by CORT. Thus, based on this study and previous reports we propose that both TCR-mediated signals and glucocorticoids are important physiological regulators of CD4 expression. In addition, these findings may be of significance for the sensitivity of CD4+ cells to HIV infection upon T cell activation, as the efficacy of primary patient HIV entry depends on the level of surface CD4.

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Glucocorticoids and Immune Function

Cited by 165 publications

References 0 publications

TCR signaling inhibits glucocorticoid-induced apoptosis in murine thymocytes depending on the stage of development

TCR signaling inhibits glucocorticoid-induced apoptosis in murine thymocytes depending on the stage of development

Leptin Is an Endogenous Protective Protein against the Toxicity Exerted by Tumor Necrosis Factor

Glucocorticoids Regulate TCR-Induced Elevation of CD4: Functional Implications

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