Antigen dose‐dependent suppression of murine IgE responses is mediated by CD4<sup>−</sup>CD8<sup>−</sup> double‐negative T cells

Barwig, Christina; Raker, Verena; Montermann, Evelyn; Grabbe, Stephan; Reske‐Kunz, Angelika B.; Sudowe, Stephan

doi:10.1111/j.1365-2222.2010.03476.x

Cited by 10 publications

(6 citation statements)

References 49 publications

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“…This was associated with decreased eosinophil recruitment, decreased Th2 cytokines to recall in vitro stimulation, and reduction in sera IgE levels. Consistent with our findings, Aguilar-Pimentel et al and others have shown that hi-dose intraperitoneal sensitization leads to modulation of Th2 in the allergic asthma model [12]. Data herein suggest that this effect in our model was not associated with a dominant Th1 response, as hi-dose sensitization was found here to have suppressed IFN-g levels indicated by recall stimulation of LN T cells in vitro.…”

Section: Discussionsupporting

confidence: 93%

“…HI-dose intraperitoneal sensitization in mice is a highly reproducible model to induce an impairment of allergic Th2 responses [6-12], and thereby is of particular utility toward elucidation of natural mechanisms that modulate allergy. Evidence has led to the hypothesis that such an altered response is merely a secondary effect of priming a Th1 dominant response—which in turn suppresses other Th subsets such as Th2 [6-8].…”

Section: Introductionmentioning

confidence: 99%

“…Evidence has led to the hypothesis that such an altered response is merely a secondary effect of priming a Th1 dominant response—which in turn suppresses other Th subsets such as Th2 [6-8]. However, there are a number of studies that have challenged this dogma with the observation that an increased Th1 response was not observed in response to hi-dose intraperitoneal sensitization [9-12]. Furthermore, it is now widely appreciated that allergic immune responses are contributed to by other Th subsets such as Th1 and Th17 [13-17].…”

Section: Introductionmentioning

confidence: 99%

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Ocular Allergy Modulation to Hi-Dose Antigen Sensitization Is a Treg-Dependent Process

et al. 2013

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A reproducible method to inhibit allergic immune responses is accomplished with hi-dose Ag sensitization, via intraperitoneal (IP) injection. However, the role of CD4+ CD25+ FoxP3+ T regulatory cells (Treg) in this process is unknown, as is whether such modulation extends to ocular allergy. We therefore determined herein whether hi-dose sensitization modulates ocular allergy, and whether CD4+ CD25+ FoxP3+ Treg are involved. C57BL/6 mice were IP sensitized via low-dose (100 µg) versus hi-dose (1000 µg) ovalbumin (OVA), in aluminum hydroxide (1 mg) and pertussis-toxin (300 ng). Other mice received anti-CD25 Ab (PC61) to ablate Treg during sensitization. In another experiment, Treg from hi-dose sensitized mice were adoptively transferred into low-dose sensitized mice. Once daily OVA challenges were administered. Clinical signs, IgE, T cell cytokines, and eosinophils were assessed. Data revealed that hi-dose, but not low-dose, sensitization led to allergy modulation, indicated by decreased clinical signs, serum IgE levels, Th2 recall responses, and eosinophil recruitment. T cells from hi-dose sensitized mice showed a robust increase in TGF-b production, and Treg from these mice were able to efficiently suppress effector T cell proliferation in vitro. In addition, in vivo Treg ablation in hi-dose sensitized mice revoked allergy modulation. Lastly, Treg from hi-dose sensitized mice were able to adoptively transfer allergy modulation to their low-dose sensitized counterparts. Collectively, these findings indicate that modulation to hi-dose sensitization, which is extended to ocular allergy, occurs in a Treg-dependent manner. In addition, our data suggest that hi-dose sensitization may henceforth facilitate the further examination of CD4+ CD25+ FoxP3+ Treg in allergic disease.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Ocular Allergy Modulation to Hi-Dose Antigen Sensitization Is a Treg-Dependent Process

et al. 2013

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“…Low exposure is likely to be one of the reasons. A weak antigen signal is known to instruct dendritic cells to signal T cells to initiate a TH2‐polarized response (75, 76) and affects another T‐cell population as well (77). This would have an effect on the B‐cell response to the antigen as a whole, but not necessarily at the level of B‐cell paratope specificity.…”

Section: Techniques To Identify (Partial) Epitopesmentioning

confidence: 99%

IgE-binding epitopes: a reappraisal

Aalberse

Crameri

2011

Allergy

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To cite this article: Aalberse RC, Crameri R. IgE‐binding epitopes: a reappraisal. Allergy 2011; 66: 1261–1274. Abstract Here, we discuss various questions related to IgE epitopes: What are the technical possibilities and pitfalls, what is currently known, how can we put this information into hypothetical frameworks and the unavoidable question: how useful is this information for patient care or allergenicity prediction? We discuss the information obtained by (i) 3D structures of allergen–antibody complexes; (ii) analysis of allergen analogues; (iii) mimics without obvious structural similarity; (iv) mAbs competing with IgE; (v) repertoire analysis of cloned IgEs, and other developments. Based on limited data, four suggestions are presented in the literature: (i) IgE might be more cross‐reactive than IgG; (ii) IgE might be more often directed to immunologically ‘uninviting’ surfaces; (iii) IgE epitopes may tend to cluster and (iv) IgE paratopes might have a higher intrinsic flexibility. While these are not proven facts, they still can generate hypotheses for future research. The hypothesis is put forward that the IgE repertoire of switched B‐cells is less influenced by positive selection, because positive selection might not be able to rescue IgE‐switched B cells. While this might be of interest for the discussion about mechanisms leading to allergen‐sensitization, we need to be modest in answering the ‘clinical relevance’ question. Current evidence indicates the IgE‐epitope repertoire is too big to make specific IgE epitopes a realistic target for diagnosis, treatment or allergenicity prediction. In‐depth analysis of a few selected IgE epitope‐peptides or mimitopes derived from allergen‐sequences and from random peptide libraries, respectively, might well prove rewarding in relation to diagnosis and prognosis of allergy, particularly food allergy.

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“…They found little difference in the response to crude peanut extract between peanut allergic and peanut sensitized children with Th1 and Th2 cytokine production from both, but allergic children had enhanced responses to purified allergens [58]. Further insight into the mechanisms involved in sensitization and particularly the effect of the dose of allergen was provided by Barwig et al [59]. They compared in a mouse model of sensitization to keyhole limpet antigen, the effect of a high and low dose of allergen on sensitization.…”

Section: Th Cellsmentioning

confidence: 99%

Developments in the field of allergy in 2010 through the eyes of Clinical and Experimental Allergy

Katelaris

Linneberg

Magnan

et al. 2011

Clin Experimental Allergy

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In 2010 over 200 articles were published in Clinical and Experimental Allergy including editorials, reviews, opinion articles, letters, book reviews and of course at the heart of the journal, papers containing original data which have moved the field of allergy forward on a number of fronts. For the third year running the editors felt it would be of value to summarize the key messages contained in these papers as a snapshot of where the cutting edge of research into allergic disease is leading. We have broadly followed the sections of the journal, although this year the mechanistic articles are grouped together and the studies involving experimental models of disease are discussed throughout the paper. In the field of asthma and rhinitis phenotypes and biomarkers continue to a major pre-occupation of our authors. There is continued interest in mechanisms of inflammation and disordered lung function with the mouse model of asthma continuing to offer new insights. There is also a steady flow of papers investigating new therapies, including those derived from plants and herbs, although many are mechanistic with too few high quality clinical trials. The mechanisms involved in allergic disease are well covered with many strong papers using clinical material to ask relevant questions. Pro-pre and snybiotics continue to be of major interest to our authors and this remains a controversial and complicated field. The discipline of epidemiology has retained its interest in risk factors for the development of allergic disease with a view to refining and debating the reasons for the allergy epidemic. There is continued interest in the relationship between helminthic disease and allergy with a new twist in 2010 involving studies using infection with helminths as a potential treatment. The genetics of allergic disease continues to be very productive, although the field has moved on from only investigating single nucleotide polymorphisms of candidate genes to Genome Wide Association Studies and an increasing and welcome emphasis on gene-environment interactions. In the field of clinical allergy there is steady flow of papers describing patterns of drug allergy with renewed interest in reactions to contrast media, but food allergy is the major area of interest in this section of the journal. Lastly in the field of allergens there is a growing interest in the role of component resolved diagnosis in improving the diagnosis and management of allergic disease. Another excellent year, full of fascinating and high quality work, which the journal has been proud to bring to the allergy community.

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Antigen dose‐dependent suppression of murine IgE responses is mediated by CD4⁻CD8⁻ double‐negative T cells

Abstract: Our data demonstrate that CD4(-)CD8(-) dnT cells play a major role in the regulation of IgE responses induced by high antigen doses.

Cited by 10 publications

References 49 publications

Ocular Allergy Modulation to Hi-Dose Antigen Sensitization Is a Treg-Dependent Process

Ocular Allergy Modulation to Hi-Dose Antigen Sensitization Is a Treg-Dependent Process

IgE-binding epitopes: a reappraisal

Developments in the field of allergy in 2010 through the eyes of Clinical and Experimental Allergy

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Antigen dose‐dependent suppression of murine IgE responses is mediated by CD4−CD8− double‐negative T cells

Abstract: Our data demonstrate that CD4(-)CD8(-) dnT cells play a major role in the regulation of IgE responses induced by high antigen doses.

Cited by 10 publications

References 49 publications

Ocular Allergy Modulation to Hi-Dose Antigen Sensitization Is a Treg-Dependent Process

Ocular Allergy Modulation to Hi-Dose Antigen Sensitization Is a Treg-Dependent Process

IgE-binding epitopes: a reappraisal

Developments in the field of allergy in 2010 through the eyes of Clinical and Experimental Allergy

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Product

Resources

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Antigen dose‐dependent suppression of murine IgE responses is mediated by CD4⁻CD8⁻ double‐negative T cells