Dependence of mast cell IgE-mediated cytokine production on nuclear factor-κB activity

Marquardt, Diana L.; Walker, Linda L.

doi:10.1067/mai.2000.104942

Cited by 124 publications

(102 citation statements)

References 28 publications

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“…S4B, C). Consistent with this, BAPTA prevented the generation of IL-1␤, IL-3, IL-6, TNF-␣, MIP-2, MCP-1, and MIP-1␣ synthesis, which are dependent on NF-B activity (27), whereas BAPTA had no effect on IL-33-triggered IL-5, IL-13, Eotaxin-2, RANTES or TARC syntheses, which are independent of the NF-B pathway (28) (Figs. S5D, E).…”

Section: Il-33 Triggered Calcium-dependent Activation Of Nf B Cytokinesupporting

confidence: 59%

“…It has been suggested that whilst the production of pro-inflammatory cytokines in mast cells is NF B (p50 and p65) dependent (27)(28)(29), the induction of Th2 cytokines is NF B independent (30) . We therefore investigated the effect of IL-33 on the activation of NF B and MAPKs in human mast cells.…”

Section: Il-33 Triggered Calcium-dependent Activation Of Nf B Cytokinementioning

confidence: 99%

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RETRACTED: The cytokine interleukin-33 mediates anaphylactic shock

Pushparaj

Tay

H'ng

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

269

233

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Anaphylactic shock is characterized by elevated immunoglobulin-E (IgE) antibodies that signal via the high affinity Fcε receptor (FcεRI) to release inflammatory mediators. Here we report that the novel cytokine interleukin-33 (IL-33) potently induces anaphylactic shock in mice and is associated with the symptom in humans. IL-33 is a new member of the IL-1 family and the ligand for the orphan receptor ST2. In humans, the levels of IL-33 are substantially elevated in the blood of atopic patients during anaphylactic shock, and in inflamed skin tissue of atopic dermatitis patients. In murine experimental atopic models, IL-33 induced antigen-independent passive cutaneous and systemic anaphylaxis, in a T cell–independent, mast cell–dependent manner. In vitro , IL-33 directly induced degranulation, strong eicosanoid and cytokine production in IgE-sensitized mast cells. The molecular mechanisms triggering these responses include the activation of phospholipase D1 and sphingosine kinase1 to mediate calcium mobilization, Nuclear factor–κB activation, cytokine and eicosanoid secretion, and degranulation. This report therefore reveals a hitherto unrecognized pathophysiological role of IL-33 and suggests that IL-33 may be a potential therapeutic target for anaphylaxis, a disease of considerable unmet medical need.

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Section: Il-33 Triggered Calcium-dependent Activation Of Nf B Cytokinesupporting

confidence: 59%

Section: Il-33 Triggered Calcium-dependent Activation Of Nf B Cytokinementioning

confidence: 99%

RETRACTED: The cytokine interleukin-33 mediates anaphylactic shock

Pushparaj

Tay

H'ng

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

269

233

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“…4 IgE-dependent mast cell activation plays an important role in the development of allergy. The cross-linking of allergen-specific IgE bound to its high-affinity receptor, FceRI, results in a series of molecular events leading to nuclear factor (NF)-kB activation 5,6 and subsequent cytokine production. Many mast cell-derived cytokines, including tumor necrosis factor-a (TNF-a), are regulated by the transcription factor NF-kB.…”

Section: Introductionmentioning

confidence: 99%

Association of tumor necrosis factor-α –308G>A polymorphism with IgE-mediated allergy to betalactams in an Italian population

Guéant-Rodriguez

Viola³

et al. 2007

Pharmacogenomics J

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Tumor necrosis factor-a (TNF-a) is released from mast cells via an immunoglobulin E (IgE)-dependent mechanism. The variant G4A at -308 of TNFA is part of an extended haplotype HLA-A1-B8-DR3-DQ2 and influences the gene expression. We evaluated this variant in relation to IgEmediated reactions to betalactams, in 427 subjects, including 167 cases and 260 age-and gender-paired controls. TNFA GG genotype was a significant independent predictor of the primary risk of betalactam allergy, concurrently with total IgE level, with an age-and sex-adjusted odds ratio estimated at 2.45 (95% confidence interval: 1.18-5.08, P ¼ 0.0163). Cases with -308AA genotype had a higher serum level of specific IgE than those with -308GA/ GG genotype, with median levels (relative units) of 4.6 (inter-quartiles: 3.9-10.6) and 2.2 (1.4-4.3), respectively (P ¼ 0.0046). In conclusion, our results suggest an ambivalent influence of a genetic determinant of pro-inflammatory pathways on IgE-mediated hypersensitivity to betalactams.

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“…PKD is abundant in mast cells and, when activated upon FcεRI engagement, it contributes to the regulation of transcriptional activity of NF-κB (Johannes et al, 1998). NFκB activation was observed upon FcεRI aggregation in mast cells (Hundley, Blood, 2004) and dendritic cells (Kraft et al, 2002), preceded by the seryl-phopshorylation and degradation of IκB, and it was reported to be involved in the generation of several cytokines (Marquardt and Walker, 2000). NF-κB was also activated in human monocytes (Drechsler et al, 2002) and mesangial cells (Duque et al, 1997), as a consequence of FcγRs and FcαRI aggregation, respectively.…”

Section: Intracellular Propagation Of Fcr Signalsmentioning

confidence: 99%

Negative Signaling in Fc Receptor Complexes

Daëron

Lesourne

2006

Advances in Immunology

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Cell activation results from the transient displacement of an active balance between positive and negative signaling. This displacement depends in part on the engagement of cell surface receptors by extracellular ligands. Among these are Receptors for the Fc portion of immunoglobulins (FcRs). FcRs are widely expressed by cells of hematopoietic orign. When binding antibodies, FcRs provide these cells with immunoreceptors capable of triggering numerous biological responses in response to specific antigen. FcR-dependent cell activation is regulated by negative signals which are generated together with positive signals within signalosomes that form upon FcR engagement. Many molecules involved in positive signaling, including the FcRβ subunit, the src kinase lyn, the cytosolic adapter Grb2, the transmembrane adapters LAT and NTAL, are indeed also involved in negative signaling. A major player in negative regulation of FcR signaling is the inositol 5-phosphatase SHIP1. Several layers of negative regulation operate sequentially as FcRs are engaged by extracellular ligands of increasing valency. A background protein tyrosine phosphatasedependent negative regulation maintains cells in a « resting » state. SHIP1-dependent negative regulation can be detected as soon as high-affinity FcRs are occupied by antibodies in the absence of antigen. It increases when activating FcRs are engaged by multivalent ligands and, further when FcR aggregation increases, accounting for the bell-shaped dose-response curve observed in excess of ligand. Finally, F-actin skeleton-associated high-molecular weight SHIP1, recruited to phopshorylated ITIMs, concentrates in signaling complexes when activating FcRs are coengaged with inhibitory FcRs by immune complexes. Based on these data, activating and inhibitory FcRs could be used for new therapeutic approaches of immune disorders.

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Dependence of mast cell IgE-mediated cytokine production on nuclear factor-κB activity

Cited by 124 publications

References 28 publications

RETRACTED: The cytokine interleukin-33 mediates anaphylactic shock

RETRACTED: The cytokine interleukin-33 mediates anaphylactic shock

Association of tumor necrosis factor-α –308G>A polymorphism with IgE-mediated allergy to betalactams in an Italian population

Negative Signaling in Fc Receptor Complexes

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