Glucocorticoids increase the synthesis of immunoglobulin E by interleukin 4-stimulated human lymphocytes.

Cy, Wu; Sarfati, Marika; Heusser, C.; Fournier, Sylvie; Rubio-Trujillo, M; Peleman, Renaat; Delespesse, Guy

doi:10.1172/jci115092

Cited by 153 publications

(79 citation statements)

References 36 publications

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“…However, since progesterone is unable to induce IgE synthesis in IL-4-stimulated PBMCs (ref. 22 and data not shown), these results suggest that GR is critical for upregulation of CD40L mRNA and for induction of IgE synthesis by HC.…”

mentioning

confidence: 65%

“…Similar results were obtained with DM, which has relatively more pure GC activity than HC (data not shown). Progesterone, which fails to induce IgE synthesis in IL-4-stimulated B cells (22), failed to upregulate CD40L mRNA expression (data not shown).…”

Section: Figurementioning

confidence: 88%

“…ethasone (DM), but not mineralocorticoids or sex steroids, induce in the presence of IL-4 IgE synthesis by human B cells (21,22). This was shown to involve deletional switch recombination (23).…”

mentioning

confidence: 99%

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

Jabara¹,

Brodeur²,

Geha³

2001

J. Clin. Invest.

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confidence: 65%

Section: Figurementioning

confidence: 88%

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

Jabara¹,

Brodeur²,

Geha³

2001

J. Clin. Invest.

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“…Several groups have concluded that CS strongly potentiate IL-4-induced IgE synthesis by PBMC in vitro (25)(26)(27)(28), such that supplementation of culture medium with CS actually supplants the need for concomitant T cell help in IgE isotype switching (29). Using B cells from allergic patients, Bohle et al (30) have shown that this CS-mediated IgE production is polyclonal and cannot be attributed to the selective enhancement of allergen-specific IgE.…”

Section: Figurementioning

confidence: 99%

Transient Corticosteroid Treatment Permanently Amplifies the Th2 Response in a Murine Model of Asthma

Wiley

Cwiartka

Álvarez

et al. 2004

The Journal of Immunology

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Corticosteroids (CS) remain the most efficacious pharmacotherapeutic option for the management of asthma. Although the acute anti-inflammatory effects of CS treatment have been amply documented both clinically and experimentally, recent human data intimate that exposure to CS may be associated with retrograde immune phenomena, including enhanced synthesis of IgE in vivo and elevated Th2 cytokine production in vitro. We have investigated the long-term immunologic effects of CS treatment in a murine model of allergic airway inflammation. CS treatment during initial exposure to OVA or upon long-term Ag rechallenge remarkably attenuated eosinophilic airway inflammation and airway hyperresponsiveness. Interestingly, however, Th2 cytokine production by cultured splenocytes from CS-treated mice was significantly elevated, while IFN-γ synthesis was depressed. Moreover, mice rechallenged with OVA several weeks after CS intervention during allergic sensitization not only developed airway inflammation, but also exhibited enhanced Th2 cytokine production in lymphoid tissues and OVA-specific IgE in serum. This amplification of the systemic immune response was associated with an intact APC compartment during CS-conditioned sensitization to OVA. These data indicate that immune processes underlying the allergic phenotype remain impervious to CS treatment and raise the possibility that treatment with CS during sensitization may amplify elements of the allergen-specific immune response.

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“…National Sagamihara Hospital, 18-1 Sakuradai, Sagamiiiara City, iCanagawa 228, Japan, 0 1995 Blackwell Science IgE production. This signal can be provided not only by activated CD4^ T cells [9,10], but also by Epstein Barr virus (EBV) infeclion [11], hydrocortisone [12,13], anti-CD40 MoAb [10,14]. CD40 ligand [15] or anti-CD58 MoAb [16].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of IL-4 receptor up-regulation on B cells by antisense oligodeoxynucleotide suppresses IL-4-induced human IgE production

Ikizawa

Kondo

Koshio

et al. 1995

Clinical and Experimental Immunology

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SUMMARYlL-4 is shown to up-regulate its own receptor (IL-4R) on human lymphocytes, but the functional significance of up-regulated IL-4R is not clear regarding IgE production. This study investigated the possible role of IL-4-induced up-regulation of IL-4R on B cells in the induction ofhuman IgE synthesis by means of antisense strategy. Among three antisense oligodeoxynucleotides designed against the downstream of translation initiation siteof 1L-4R cDNA. S-oligo [.complementary to nucleotide 1-24, showed the strongest inhibition ofthe constitutive expression of IL-4R on Daudi cells. Addition of S-oligo ! together with IL-4 also decreased the up-regulated but not constitutive levels of IL-4R on peripheral blood B cells without affecting the concomitant enhancement of CD23, CD40, HLA-DR and surface IgM expression, indicating that ils effect is specific for IL-4R up-regulation. When S-oligo 1 was added to B cells costimulated with IL-4 and anti-CD40 MoAb, it induced a dose-dependent inhibition of IgE production. This inhibition was accompanied by a decrease in the expression of mature C< transcripts, whereas the accumulation of germ-line O transcripts was not affected by S-oligo 1. These data suggest that the signal transduclion mediated by the up-regulated IL-4R on B cells may be intimately associated with the induction of isotype switching to IgE thai leads to mature Ce transcription and IgE production.

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Glucocorticoids increase the synthesis of immunoglobulin E by interleukin 4-stimulated human lymphocytes.

Abstract: This study indicates that hydrocortisone (HC) Clin. Invest. 1991. 87:870-877.)

Cited by 153 publications

References 36 publications

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

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

Transient Corticosteroid Treatment Permanently Amplifies the Th2 Response in a Murine Model of Asthma

Inhibition of IL-4 receptor up-regulation on B cells by antisense oligodeoxynucleotide suppresses IL-4-induced human IgE production

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