Glucocorticoids accelerate anti T-cell receptor stimulated growth of rat spleen T-cells

Wiegers, G. Jan; Labeur, Marta; Stec, IE; Holsboer, Florian; Reul, Johannes M. H. M.

doi:10.1016/0165-5728(94)90583-5

Cited by 46 publications

(82 citation statements)

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“…Nonetheless, the induction of CD4 by glucocorticoids is not the only mechanism by which these hormones augment proliferation, as saturating concentrations of inhibitory anti-CD4 mAb in the presence of CORT did not completely reduce the proliferative response to control levels. Accordingly, among other mediators, the (direct or indirect) induction of CD25 by CORT (40) probably plays, in concert with enhanced CD4 expression, an important role in the CORT-evoked enhancement of T cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…It has been previously shown that CORT accelerates T cell proliferation in parallel with an increased IL-2R␣ expression (40). Because CD4 enhances the activation and proliferation that follow TCR engagement, the CORT-evoked acceleration of CD4 after 48 h may participate in the enhancement of T cell activation by this hormone.…”

Section: Cort-evoked Acceleration Of Cd4 Induction Is Paralleled By Imentioning

confidence: 99%

“…Both the inhibitory and stimulatory effects of CORT on T cell mitogenesis have been shown to be reversed by the glucocorticoid receptor antagonist RU486 (39,40). Next, we tested whether the effects of CORT on CD4 expression were mediated by the glucocorticoid receptor.…”

Section: The Effects Of Cort On Cd4 Expression Are Reversed By Ru486mentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Cort-evoked Acceleration Of Cd4 Induction Is Paralleled By Imentioning

confidence: 99%

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Glucocorticoids Regulate TCR-Induced Elevation of CD4: Functional Implications

Wiegers

Stec

Klinkert

et al. 2000

The Journal of Immunology

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“…GCs decrease IL-2 production, but they expedite expression of the IL-2 receptor. The result is that acute stress-levels of GCs enhance T cell proliferation by accelerating the ability of IL-2 to signal through its receptor (Wiegers et al 1995;Almawi et al 1999). Notably, exposure to chronic, high levels of corticosterone prevented this effect (Sterzer et al 2004).…”

Section: The Pro-inflammatory Effects Of Gcs Outside the Nervous Systemmentioning

confidence: 99%

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

389

283

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In recent years the classic view that glucocorticoids, the adrenal steroids secreted during stress, are universally anti-inflammatory has been challenged at a variety of levels. It was first observed that under some circumstances, acute GC exposure could have pro-inflammatory effects on the peripheral immune response. More recently, chronic exposure to GCs has been found to have pro-inflammatory effects on the specialized immune response to injury in the central nervous system. Here we review the evidence that in some cases, glucocorticoids can increase pro-inflammatory cell migration, cytokine production, and even transcription factor activity in the brain. We consider how these unexpected effects of glucocorticoids can co-exist with their well-established anti-inflammatory properties, as well as the considerable clinical implications of these findings.

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“…Thus, GC can inhibit the production of a cytokine, enhance the expression of its receptor and potentiate its biological effect. The net outcome of these paradoxical effects may result in an enhanced immune response both in vivo [6] and in vitro [7][8][9].…”

Section: Introductionmentioning

confidence: 99%