In vivo effects of glucocorticoids on IgE production

Zieg,; Lack,; Harbeck,; Gelfand,; Leung,

doi:10.1053/ai.1994.v94.a54936

Cited by 100 publications

(41 citation statements)

References 21 publications

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“…First, corticosteroids have been shown to potentiate IL-4-induced polyclonal IgE synthesis by peripheral blood B cells in vitro (32-36). In vivo, corticosteroid treatment has been shown to increase serum IgE levels transiently (37,38). In addition, corticosteroid therapy has been shown to potentiate Th2 differentiation, by either reducing IL-12 secretion from APC (6 -8, 39 -43) or by directly suppressing Th1 cell polarization (44).…”

Section: Discussionmentioning

confidence: 99%

Respiratory Tolerance Is Inhibited by the Administration of Corticosteroids

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Akbari

Umetsu

2005

The Journal of Immunology

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Corticosteroids constitute the most effective current anti-inflammatory therapy for acute and chronic forms of allergic diseases and asthma. Corticosteroids are highly effective in inhibiting the effector function of Th2 cells, eosinophils, and epithelial cells. However, treatment with corticosteroids may also limit beneficial T cell responses, including respiratory tolerance and the development of regulatory T cells (TReg), which actively suppress inflammation in allergic diseases. To examine this possibility, we investigated the effects of corticosteroid administration on the development of respiratory tolerance. Respiratory exposure to Ag-induced T cell tolerance and prevented the subsequent development of allergen-induced airway hyperreactivity. However, treatment with dexamethasone during the delivery of respiratory Ag prevented tolerance, such that allergen sensitization and severe airway hyperreactivity subsequently occurred. Treatment with dexamethasone during respiratory exposure to allergen eliminated the development of IL-10-secreting dendritic cells, which was required for the induction of IL-10-producing allergen-specific TReg cells. Therefore, because allergen-specific TReg cells normally develop to prevent allergic disease and asthma, our results suggest that treatment with corticosteroids, which limit the development of TReg cells and tolerance to allergens, could enhance subsequent Th2 responses and aggravate the long-term course of allergic diseases and asthma.

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Section: Discussionmentioning

confidence: 99%

Respiratory Tolerance Is Inhibited by the Administration of Corticosteroids

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Akbari

Umetsu

2005

The Journal of Immunology

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“…In addition to inducing IgE synthesis in vitro, administration of GCs has been reported to result in a significant rise in serum IgE in patients with asthma but not in normal nonatopic subjects (41,42). This discrepancy may reflect the fact that induction of IgE synthesis by GCs requires IL-4, and IL-4 is detected in cells and serum of atopic patients but not of nonatopic controls (43)(44)(45)(46)(47).…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids upregulate CD40 ligand expression and induce CD40L-dependent immunoglobulin isotype switching

Jabara¹,

Brodeur²,

Geha³

2001

J. Clin. Invest.

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“…Despite the overall suppressive effect on T cell cytokine production, glucocorticoid treatment has been shown to result in increased IgE production in vivo (6,51). The effects of glucocorticoids on accessory monocytes may provide insight into this seemingly paradoxical response.…”

Section: Discussionmentioning

confidence: 99%

Cooperation Among Stat1, Glucocorticoid Receptor, and PU.1 in Transcriptional Activation of the High-Affinity Fcγ Receptor I in Monocytes

Aittomäki¹,

Pesu

Groner

et al. 2000

The Journal of Immunology

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IFN-γ and glucocorticoids regulate inflammatory and immune responses through Stat1 and glucocorticoid receptor (GR) transcription factors, respectively. The biological responses to these polypeptides are determined by integration of various signaling pathways in a cell-type and promoter-dependent manner. In this study we have characterized the molecular basis for the functional cooperation between IFN-γ and dexamethasone (Dex) in the induction of the high-affinity Fcγ receptor I (FcγRI) in monocytes. Dex did not affect IFN-γ-induced Stat1 DNA binding activity or induce novel DNA-binding complexes to the FcγRI promoter. By using cell systems lacking functional GR or Stat1, we showed that GR stimulated Stat1-dependent transcription in a ligand-dependent manner, while Stat1 did not influence GR-dependent transcription. The cooperation required phosphorylation of Tyr701, DNA binding, and the trans-activation domain of Stat1, but did not involve Ser727 phosphorylation of Stat1 or physical interaction between GR and Stat1. The costimulatory effect of Dex was not dependent on a consensus glucocorticoid response element in the Stat1-responsive promoters, but required the DNA-binding and trans-activation functions of GR, and Dex-induced protein synthesis. GR activated the natural FcγRI promoter construct, and this response required both Stat1 and the Ets family transcription factor PU.1. Previously, physical association between GR and Stat5 has been shown to enhance Stat5-dependent and suppress GR-dependent transcription. The results shown here demonstrate a distinct, indirect mechanism of cross-modulation between cytokine and steroid receptor signaling that integrates Stat1 and GR pathways with cell type-specific PU.1 transcription factor in the regulation of FcγRI gene transcription.

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In vivo effects of glucocorticoids on IgE production

Cited by 100 publications

References 21 publications

Respiratory Tolerance Is Inhibited by the Administration of Corticosteroids

Respiratory Tolerance Is Inhibited by the Administration of Corticosteroids

Glucocorticoids upregulate CD40 ligand expression and induce CD40L-dependent immunoglobulin isotype switching

Cooperation Among Stat1, Glucocorticoid Receptor, and PU.1 in Transcriptional Activation of the High-Affinity Fcγ Receptor I in Monocytes

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