Allergen extract‐induced interleukin‐10 in human memory B cells inhibits immunoglobulin E production

Milovanović, M; Heine, Guido; Zuberbier, Torsten; Worm, Margitta

doi:10.1111/j.1365-2222.2009.03233.x

Cited by 19 publications

(16 citation statements)

References 45 publications

(44 reference statements)

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“…In addition, low IL-10 production early in life has been associated with the development of atopic dermatitis [15] . Our findings of rapid effects at the level of PBMCs are in agreement with previous reports on immunological responses to allergoid-SIT already after a few injections [16] , and are likewise compatible with allergen-specific IL-10 responses in B cells [17] .…”

Section: Discussionsupporting

confidence: 82%

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The Impact on Allergy-Related Cells of a Birch Pollen Allergoid, with and without Monophosphoryl Lipid A, in Comparison with the Native Equivalent

Worm

Ernst²,

Kraller³

et al. 2017

Int Arch Allergy Immunol

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Background: The clinical efficacy and safety of allergoid immunotherapy have been demonstrated in clinical trials. However, simultaneous monitoring of the immunological changes by allergoids versus allergens in the cells of the same individual has not been extensively performed, and the impact of concurrent Toll-like receptor 4 (TLR4) ligation has not been specified. Methods: Three types of birch allergen were utilized: glutaraldehyde-treated allergoid (extract A), the same allergoid plus monophosphoryl lipid A (MPL), i.e., TLR4 ligand (extract A*), and native allergen (extract B). Antigen-specific responses after the in vitro stimulation of blood cells with the extracts were assessed by studying costimulatory receptors on the B cell surface by flow cytometry, cytokine responses by ELISA, and CD63 and CD203c upregulation (basophil activation test) in allergic versus nonallergic subjects. Results: HLA-DR selectively increased upon allergen or allergoid treatment in the allergic group only. The extract types elicited similar cytokine responses, with IL-6 and IL-10 production detected only in certain atopic subjects. The allergoids revealed a strong reduction (100- to <10,000-fold) in basophil activation versus native allergen. Reactivity was undetectable in the basophils from nonallergic subjects. Conclusion: The allergenicity of the allergoid employed was sharply reduced when compared to the native allergen, while its immunogenicity was largely retained, especially in the presence of MPL. We also provide further evidence that allergic and nonallergic individuals show preexisting differences in their immune repertoires.

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Section: Discussionsupporting

confidence: 82%

“…This is supported by the reported correlation between allergen-specific IgE responses and T cell proliferation induced by the same allergen, while recall responses to tetanus toxoid display no such correlation [18] . In addition, direct effects on allergenspecific B cells may also contribute to the overall response [17,19] .…”

Section: Discussionmentioning

confidence: 99%

The Impact on Allergy-Related Cells of a Birch Pollen Allergoid, with and without Monophosphoryl Lipid A, in Comparison with the Native Equivalent

Worm

Ernst²,

Kraller³

et al. 2017

Int Arch Allergy Immunol

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show abstract

“…The induction of T regs and IL-10 secretion from dendritic cells was thought to underlie the effectiveness of 1,25(OH) 2 D to suppress immune mediated disease (33–35). 1,25(OH) 2 D induced the production of IL-10 in human B cells and IL-10 production by human memory B cells inhibited IgE production in vitro (36, 37). In addition, there may be IL-10 independent effects of 1,25(OH) 2 D on IgE class switching (29, 30).…”

Section: Discussionmentioning

confidence: 96%

Control of Circulating IgE by the Vitamin D Receptor In Vivo Involves B Cell Intrinsic and Extrinsic Mechanisms

James

Weaver

Cantorna

2017

The Journal of Immunology

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Vitamin D deficiency is associated with the development of asthma and allergy. The active form of vitamin D (1,25(OH)2D) regulates B cells in vitro and mice without the vitamin D receptor (VDR KO) have high serum IgE. Whole body VDR KO, T-VDR KO, B-VDR KO and vitamin D deficient mice were used to determine the targets of vitamin D in the regulation of IgE in vivo. Vitamin D deficient, VDR KO and B-VDR KO mice developed hyper-IgE, while T-VDR KO mice did not. The data show that IL-10 secretion by B cells and CD1d expression on B10 cells was lower in VDR KO mice. Mesenteric lymph node cultures from VDR KO and B-VDR KO mice secreted higher IgE ex vivo than WT cultures, and the addition of IL-10 eliminated the difference in IgE production between VDR KO and WT cultures. The increase in IgE in VDR KO mice was 2-fold greater than in the B-VDR KO mice suggesting that VDR deficiency in non-B cells contributes to hyper-IgE in vivo. Antibiotic depletion of the microbiota raised serum IgE 4-fold in both WT and VDR KO mice. The VDR directly and indirectly regulates IgE production in B cells. Vitamin D, through the VDR, is an environmental factor that helps to maintain low serum IgE responses.

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“…Nonallergic and allergic donors are characterized in Table 1. After density gradient centrifugation using Ficoll and two washing steps with phosphate-buffered saline, cells were labeled with anti-CD19 beads, washed, and positively selected to 499% purity by magnetic sorting (Miltenyi, Bergisch Gladbach, Germany) as described previously (Milovanovic et al, 2009). B cells or PBMCs (10 6 per ml) were cultured in flat-bottomed 48-well plates in Roswell's Park Memorial Institute 1640 medium supplemented with 10% heat-inactivated fetal calf serum, glutamine (2 mM), penicillin (100 U ml À1 ), and streptomycin (100 mg ml À1 ) (all from Biochrom, Berlin, Germany).…”

Section: Methodsmentioning

confidence: 99%

Interleukin-17A Promotes IgE Production in Human B Cells

Milovanović

Drozdenko

Weise

et al. 2010

Journal of Investigative Dermatology

104

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Recently the Th1/Th2 concept has been revised and Th17 cells have been implicated in allergy. Despite clear correlative evidence, the cellular and molecular basis for the connection between increased IL-17A and IgE in allergy has not been elucidated. Here we show using flow cytometry that allergic patients have higher numbers of IL-17A+ cells compared to nonallergic donors. The selective removal of IL-17A+ cells from peripheral blood mononuclear cells of allergic donors after an IL-17A secretion assay reduces IgE levels, whereas re-addition of recombinant IL-17A restores it, as measured by ELISA, showing their important functional implication for IgE production. In addition, IL-17A directly promotes the differentiation of IgE-secreting cells and IgE production upon anti-CD40/IL-4 costimulation, as shown by enzyme-linked immunospot technique and ELISA. IL-17A triggers rapid degradation of IκBα and subsequent translocation of NF-κB into the B-cell nucleus, followed by transcription of epsilon germ-line, activation-induced cytidine deaminase, and IFN regulatory factor 4, as analyzed by flow cytometry, western blot, and quantitative real-time RT-PCR, respectively. Our study shows that IL-17A+ cells promote IgE production and that IL-17A exerts its pro-allergic effect directly at the level of B cells. Therefore, IL-17A might be a target for the treatment of IgE-dependent diseases, including atopic dermatitis.

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Allergen extract‐induced interleukin‐10 in human memory B cells inhibits immunoglobulin E production

Abstract: Our data indicate that allergen-activated memory B cells can modulate IgE production through secretion of IL-10.

Cited by 19 publications

References 45 publications

The Impact on Allergy-Related Cells of a Birch Pollen Allergoid, with and without Monophosphoryl Lipid A, in Comparison with the Native Equivalent

The Impact on Allergy-Related Cells of a Birch Pollen Allergoid, with and without Monophosphoryl Lipid A, in Comparison with the Native Equivalent

Control of Circulating IgE by the Vitamin D Receptor In Vivo Involves B Cell Intrinsic and Extrinsic Mechanisms

Interleukin-17A Promotes IgE Production in Human B Cells

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