IgE in asthma and atopy: cellular and molecular connections

Oettgen, Hans C.; Geha, Raif S.

doi:10.1172/jci8205

Cited by 173 publications

(135 citation statements)

References 30 publications

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“…2-4 are from the same experiment and followed the sensitization protocol shown in Fig. 1A. cells and basophils by allergen-specific IgE leads to the release of mediators that cause allergic reactions (16). Prominent among these is histamine, an intracellular mediator of the immediate hypersensitivity response that exerts potent effects on various target tissues.…”

Section: Pn-specific Ige Correlates With Anaphylactic Symptomsmentioning

confidence: 99%

An Enteric Helminth Infection Protects Against an Allergic Response to Dietary Antigen

Bashir

Andersen

Fuss

et al. 2002

The Journal of Immunology

217

161

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Although helminths induce a polarized Th2 response they have been shown, in clinical studies, to confer protection against allergies. To elucidate the basis for this paradox, we have examined the influence of an enteric helminth infection on a model of food allergy. Upon Ag challenge, mice fed peanut (PN) extract plus the mucosal adjuvant cholera toxin (CT) produced PN-specific IgE that correlated with systemic anaphylactic symptoms and elevated plasma histamine. PN-specific IgE was not induced in helminth-infected mice fed PN without CT. Moreover, when PN plus CT was fed to helminth-infected mice, both PN-specific IgE and anaphylactic symptoms were greatly diminished. The down-regulation of PN-specific IgE was associated with a marked reduction in the secretion of IL-13 by PN-specific T cells. When helminth-infected PN plus CT-sensitized mice were treated with neutralizing Abs to IL-10, the PN-specific IgE response and anaphylactic symptoms were similar to, or greater than, those seen in mice that receive PN and CT alone. Taken together, these results suggest that helminth-dependent protection against allergic disease involves immunoregulatory mechanisms that block production of allergen-specific IgE.

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Section: Pn-specific Ige Correlates With Anaphylactic Symptomsmentioning

confidence: 99%

An Enteric Helminth Infection Protects Against an Allergic Response to Dietary Antigen

Bashir

Andersen

Fuss

et al. 2002

The Journal of Immunology

217

161

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“…I mmunoglobulin E plays a central role in the pathophysiology of allergic asthma and contributes to the inflammatory process, as indicated by findings in humans and mice that show a strong correlation between the level of IgE detected in the serum and bronchoalveolar lavage (BAL) 3 and the severity of the allergic airway inflammation that develops (1)(2)(3). Because of this correlation, the use of anti-IgE neutralizing Abs has become a very effective treatment for allergic asthma (4).…”

mentioning

confidence: 99%

The Level of IgE Produced by a B Cell Is Regulated by Norepinephrine in a p38 MAPK- and CD23-Dependent Manner

Pongratz

McAlees

Conrad

et al. 2006

The Journal of Immunology

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Although the causes of asthma vary, the severity of the disease correlates with the level of IgE produced. In this study we show that mice produced less IgE when they were depleted of the neurotransmitter norepinephrine (NE) before the administration of Ag. The suppression was prevented when a β2-adrenergic receptor (β2AR)-selective agonist was administered, suggesting that NE stimulated the β2AR to regulate the level of an IgE response in vivo. Although the cell targeted by NE to produce this effect in vivo is unknown, we show in vitro that the level of IgE increased on a per cell basis without an effect on class switch recombination when NE stimulated the β2AR on a B cell directly. The β2AR-induced increase in IgE depended on p38 MAPK but not protein kinase A activation, was due to an increased rate of mature IgE mRNA transcription, and was lost when β2AR-deficient B cells were used. Also, CD23 transcription was increased in a p38 MAPK-dependent manner and resulted in an increased level of soluble CD23 (sCD23). The β2AR-induced increase in sCD23 was associated with IgE up-regulation and possibly interacted with CD21/CD19. Using B cells from respective knockout mice, data showed that the β2AR-induced increase in IgE depended on B cell expression of CD23, CD21, and CD19. These findings suggest that at least one mechanism by which endogenous B cell activity in vivo is regulated by NE involves stimulation of the β2AR on the B cell alone to increase the level of IgE produced in a p38 MAPK- and sCD23-dependent manner.

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“…This reaction is the key to IgE-mediated allergy (4). Moreover, the expression of these high-affinity receptors is probably up-regulated by IgE itself (5,6,7). Therefore, the concentration of circulating IgE does not reflect its true activity.…”

Section: Immunoglobulin Ementioning

confidence: 99%