Successful venom immunotherapy to paper wasp, in IgE-venom negative patient
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<b><i>Background:</i></b> Protective acquired immunity against helminths and allergic sensitisation are both characterised by high IgE antibody levels. Levels of IgE antibodies are naturally tightly regulated by several mechanisms including binding of the CD23 receptor. Following observations that helminth infections and allergic sensitisation may co-present, the current study aims to investigate the relationship between the soluble CD23 (sCD23) receptor, parasite-specific IgE responses and allergic sensitisation in people exposed to the helminth parasite <i>Schistosoma haematobium</i>. <b><i>Methods:</i></b> A cohort of 434 participants was recruited in two villages with different levels of <i>S. haematobium</i> infection in Zimbabwe. Serum levels of the 25-kDa fragment of sCD23 were related to levels of schistosome infection intensity, allergen (house dust mite, HDM) and schistosome-specific IgE, total IgE and skin sensitisation to HDM. <b><i>Results:</i></b> sCD23 levels rose significantly with schistosome infection intensity but declined significantly with schistosome-specific IgE levels. Furthermore, sCD23 levels were negatively associated with skin sensitisation and IgE reactivity against HDM, but showed no relationship with total IgE. <b><i>Conclusion:</i></b> The results are consistent with the suppression of parasite and allergen-specific IgE levels by sCD23. Further mechanistic studies will determine the relevance of this potential regulatory mechanism in the development of helminth-specific immune responses in atopic individuals.
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CD23
Polyclonal antibodies
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Chronic Rhinosinusitis
Nasal Polyps
Proinflammatory cytokine
Respiratory Hypersensitivity
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Occupational exposure to chemicals is an important cause of asthma. Recent studies indicate that IgE antibodies enhance sensitization to chemicals in the skin.We investigated whether IgE might similarly promote the development of airway inflammation following inhalation of a contact sensitizer.A model of chemical-induced asthma is described in which introduction of the low-molecular-weight compound, trinitrobenzene sulphonic acid (TNBS), via the respiratory tract was used for both sensitization and challenge. The role of IgE antibodies in the immune response to inhaled TNBS in this model was assessed by comparing the responses of wild-type (WT) and IgE-deficient (IgE(-/-)) mice on the BALB/c background. Reconstitution of circulating IgE levels by intravenous injection of IgE antibodies into IgE(-/-) mice before sensitization was performed to confirm the role of IgE in any differences observed between the responses of WT and IgE(-/-) mice.Intranasal challenge of TNBS-sensitized (but not sham-sensitized control mice) induced intense pulmonary inflammation. Macrophages, eosinophils and lymphocytes, including T, B, natural killer and natural killer T cells, were recruited to the airway and the animals displayed bronchial hyperresponsiveness (BHR) to methacholine. Serum levels of murine mast cell protease-1 (mMCP-1) were elevated suggesting mast cell activation. In contrast, the development of airway inflammation, recruitment of lymphocytes, induction of BHR and production of mMCP-1 were all significantly attenuated in IgE-deficient mice. Reconstitution of IgE(-/-) mice with IgE (of unrelated antigen specificity) before sensitization partially restored these features of asthma.Our data indicate that IgE antibodies non-specifically enhance the development of airway inflammation induced by exposure to chemical antigens.
Methacholine
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The anti-IgE autoantibody in the IgG class was detected in 95.5% of patients with atopic asthma, and in 72.2% of those with non-atopic asthma, using a newly established solid phase enzyme immunoassay (EIA). The specificity of anti-IgE autoantibody was confirmed by both competitive inhibition and absorption experiments, using human IgG, IgA, IgM, IgD, IgE and rabbit anti-human IgG. Significant correlations were observed between the levels of the anti-IgE autoantibody and the serum IgE. Gel filtration studies indicated that the anti-IgE autoantibody in sera from asthmatic patients was present in the immune complex form with self-IgE, in addition to the monomeric antibody. Furthermore, this anti-IgE autoantibody has the ability to induce the reversed type immediate skin reaction, in asthma free individuals. These observations strongly suggest the putative role of the anti-IgE autoantibody in the modulation of IgE-mediated immune systems and the pathogenesis of bronchial asthma.
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Abstract Th2 responses induced by allergens or helminths share many common features. However, allergen‐specific IgE can almost always be detected in atopic patients, whereas helminth‐specific IgE is often not detectable and anaphylaxis often occurs in atopy but not helminth infections. This may be due to T regulatory responses induced by the helminths or the lack of helminth‐specific IgE. Alternatively non‐specific IgE induced by the helminths may protect from mast cell or basophil degranulation by saturating IgE binding sites. Both of these mechanisms have been implicated to be involved in helminth‐induced protection from allergic responses. An article in the current issue of the European Journal of Immunology describes the generation of an anti‐ Nippostrongylus brasiliensis ‐specific IgE antibody which was used to identify a novel N. brasiliensis antigen (Nb‐Ag1). The authors demonstrated that Nb‐Ag1 specific IgE could only be detected for a short period of time during infection, and that these levels were sufficient to prime mast cells thereby leading to active cutaneous anaphylaxis after the application of Nb‐Ag1. This is the first report clearly showing that a low level of helminth‐specific IgE, transiently produced, is able to induce mast cell degranulation in the presence of large amounts of polyclonal IgE. See accompanying article: http://dx.doi/10.1002/eji.200737135
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Using immunoblotting, we investigated sera of 60 patients with atopic dermatitis, 12 patients with helminth infections and 36 nonallergic controls, for anti-IgE autoantibodies. We found IgG anti-IgE autoantibodies in 62% of the atopics, 42% of the patients with parasitosis and 11% of the controls. IgG anti-IgE occurred most often (94%) in patients with atopic dermatitis plus additional atopic disorder, such as allergic asthma and rhinoconjunctivitis. In parallel, we found a significantly higher occurrence of IgG anti-IgE in the patients with high IgE levels compared to patients with low IgE levels (p less than 0.0005). The predominant subclasses of anti-IgE autoantibodies were IgG1 and IgG3 in atopy and parasitosis. In the controls, we found IgG4 and IgG3 anti-IgE, but no IgG1 autoantibodies. The frequency of IgG2 anti-IgE was very low; it occurred in 2 patients only. Prevalence and IgG subclass distribution of anti-IgE autoantibodies was found to be different for patients with atopic dermatitis, parasitic infection and for controls.
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Parasite immunologists had known for some time that IgE-mediated hypersensitivity reactions are rare in patients with chronic helminth infections, even though basophils and mast cells in these patients are sensitized with antiparasite IgE and exposed, often continuously, to parasite antigens. The inhibition of allergic reactivity in chronic helminth infections is mainly due to IgG4 ‘blocking antibodies’ in the serum of the infected individual. IgG4 do not fix complement and bind weakly to Fcγ receptors. Thus, antigen binding by IgG4, unlike IgE, is likely to have no or minimally harmful consequences. The discovery that, similar to IgE, expression of IgG4 is IL-4-dependent and is an intermediate step in sequential switching from IgM to IgE makes it imperative to understand how the two isotypes are coregulated and whether the two responses can be uncoupled, selectively boosting IgG4 over IgE. The ultimate goal is to apply to allergy the lesson we learnt from helminth infections.
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Allergic Inflammation
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Allergic response
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