Action of dexamethasone in the suppression of delayed-type hypersensitivity in reconstituted SCID mice

Taube, Maria Beatriz Puzzi; Carlsten, Hans

doi:10.1007/s000110050630

Cited by 12 publications

(8 citation statements)

References 28 publications

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“…The decreased survival in the presence of glucocorticoids was reversed if inducer cells were cultured in the presence of IL-7. The failure of glucocorticoids to attenuate the expression of the T cell survival signal, OX40L explain why glucocorticoids, which are effective at suppressing effector T cell responses (22,23), fail to eliminate CD4 T cell memory (24).…”

Section: Discussionmentioning

confidence: 99%

OX40 Ligand and CD30 Ligand Are Expressed on Adult but Not Neonatal CD4+CD3− Inducer Cells: Evidence That IL-7 Signals Regulate CD30 Ligand but Not OX40 Ligand Expression

Kim

Anderson²,

White³

et al. 2005

The Journal of Immunology

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In this report, we have examined the expression of the T cell survival signals, OX40 ligand (OX40L) and CD30 ligand (CD30L) on CD4+CD3−CD11c−B220−IL-7Rα+ inducer cells from birth to adulthood in mice. We found that adult but not neonatal inducer cells expressed high levels of OX40L and CD30L, whereas their expression of TNF-related activation-induced cytokine (TRANCE) and receptor activator of NF-κB (RANK) was comparable. The failure of neonatal inducer cells to express the ligands that rescue T cells helps to explain why exposure to Ag in neonatal life induces tolerance rather than immunity. The expression of OX40L and CD30L on inducer cells increased gradually in the first few weeks of life achieving essentially normal levels around the time mice were weaned. We found that IL-7 signaling through the common cytokine receptor γ-chain was critical for the optimal expression of both TNF-related activation-induced cytokine and CD30L but not OX40L. Furthermore, glucocorticoids, which potently suppress T effector function, did not influence the expression of OX40L and CD30L in the presence of IL-7.

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Section: Discussionmentioning

confidence: 99%

OX40 Ligand and CD30 Ligand Are Expressed on Adult but Not Neonatal CD4+CD3− Inducer Cells: Evidence That IL-7 Signals Regulate CD30 Ligand but Not OX40 Ligand Expression

Kim

Anderson²,

White³

et al. 2005

The Journal of Immunology

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“…It also reduced ear swelling in the CHS test, consistent with previous reports in the literature. 40 In wound healing and CHS, DEX significantly decreased induction of the Vegfr2-luc reporter; this was associated with the inhibition of inflammatory cell infiltration. Inhibition of macrophage infiltration could be the critical factor that slows angiogenesis and delays wound healing.…”

mentioning

confidence: 94%

Tracking angiogenesis induced by skin wounding and contact hypersensitivity using a Vegfr2-luciferase transgenic mouse

Zhang¹,

Fang²,

Contag³

et al. 2004

Blood

111

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The vascular endothelial growth factor-2 (VEGFR2) gene is transcriptionally regulated during angiogenesis. The ability to monitor and quantify VEGFR2 expression in vivo may facilitate a better understanding of the role of VEGFR2 in different states. Here we describe a transgenic mouse, Vegfr2-luc, in which a luciferase reporter is under control of the murine VEGFR2 promoter. In adult mice, luciferase activity was highest in lung and uterus, intermediate in heart, skin, and kidney, and lower in other tissues. Luciferase expression in these tissues correlated with endogenous VEGFR2 mRNA expression. In a cutaneous woundhealing model, Vegfr2-luc expression was induced in the wound tissue. Histologic and immunohistochemical studies showed significant macrophage infiltration into the wound and induction of Vegfr2-luc expression in endothelial and stromal cells. Dexamethasone significantly suppressed Vegfr2-luc expression and macrophage infiltration into the wound, resulting in delayed healing and impaired angiogenesis. In a skin hypersensitivity reaction produced by treatment with oxazolone, Vegfr2-luc expression was induced in the ear. Treatment by dexamethasone markedly suppressed Vegfr2-luc expression and leukocyte infiltration in the ear and was correlated with reduced dermal edema and epidermal hyperplasia. The Vegfr2-luc model will be valuable in monitoring the ability of drugs to affect angiogenesis in vivo. IntroductionAngiogenesis is the process of capillary sprouting from preexisting blood vessels. 1 The angiogenesis process is characterized by vasodilation, increased plasma leakage, remodeling of the extracellular matrix, up-regulation of growth factor receptors, proliferation and differentiation of endothelial cells, and recruitment of pericytes and smooth muscle cells, followed by the deposition of new matrix proteins for tubule formation. 2 Endothelial cells are the source of new blood vessels and have a remarkable ability to divide and migrate. A finely tuned balance between factors that activate endothelial cell growth and those that inhibit it tightly controls new capillary growth.Angiogenesis is regulated, in part, by several families of secreted growth factors that bind and activate their cognate receptors. One of the growth factors is vascular endothelial growth factor (VEGF), which exerts biologic functions through 2 related receptor tyrosine kinases: vascular endothelial growth factor receptors-1 and -2 (VEGFR1 or FLT1, and VEGFR2 or Flk1/KDR). In addition, the VEGF signaling pathway may also involve neuropilin-1 and neuropilin-2, which are used as coreceptors by VEGFR2 and VEGFR1. 3 The interaction of VEGF with its receptors is a critical part of angiogenesis. VEGFR2 mediates most of the mitogenic, survival, and vascular permeability effects of VEGF. 4,5 Angiogenesis is tightly controlled in the adult animal and occurs almost exclusively in the female reproductive system under normal conditions. 6 However, angiogenesis can be activated in adult tissues during wound healing 7 and is important in...

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“…In numerous studies intraperitoneal administration of dexamethasone even at extraordinary high concentrations was remarkably ineffective in preventing inflammation [3,[7][8][9][10][11][12][13][14][15]. While the current literature does not hold an explanation for this phenomenon, we speculate that intraperitoneally applied dex- 2.…”

mentioning

confidence: 63%

“…Interestingly, intraperitoneally applied dexamethasone was remarkably inefficient in preventing pathological changes in certain mouse models of human inflammatory diseases, even when doses up to 100 mg/kg were used [7][8][9][10][11][12][13][14]. It was therefore concluded that the glucocorticoid receptor is not an obligatory regulator of inflammation.…”

mentioning

confidence: 94%

The anti-inflammatory potency of dexamethasone is determined by the route of application in vivo

et al. 2010

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Action of dexamethasone in the suppression of delayed-type hypersensitivity in reconstituted SCID mice

Abstract: Our results indicate that corticosteroids exert suppressive impact on the effector phase of DTH response in mice by anti-inflammatory properties of the hormone or by effects on OXA-sensitised memory T cells.

Cited by 12 publications

References 28 publications

OX40 Ligand and CD30 Ligand Are Expressed on Adult but Not Neonatal CD4+CD3− Inducer Cells: Evidence That IL-7 Signals Regulate CD30 Ligand but Not OX40 Ligand Expression

OX40 Ligand and CD30 Ligand Are Expressed on Adult but Not Neonatal CD4+CD3− Inducer Cells: Evidence That IL-7 Signals Regulate CD30 Ligand but Not OX40 Ligand Expression

Tracking angiogenesis induced by skin wounding and contact hypersensitivity using a Vegfr2-luciferase transgenic mouse

The anti-inflammatory potency of dexamethasone is determined by the route of application in vivo

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