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Background Data from birth cohort studies suggest that increased cord blood total IgE and reduced cord blood regulatory T cells increase the risk of developing allergic sensitization and atopic dermatitis. Objective We here addressed whether serum total IgE and hen's egg-specific IgE levels at birth and at age 1 year differed between healthy and allergic children in a Belgian birth cohort (FONIA). We furthermore studied whether these parameters as well as cord blood Foxp3/CD3γ mRNA levels might predict the allergic outcome. Methods and results Children ( n = 84) were clinically assessed at the ages of 6, 12, 18, and 24 months and at 6 years. Cord blood total IgE levels above 0.35 kU/L predicted early (i.e. before or at the age of 2 years) allergy development. Presence of serum IgE antibodies to hen's egg (cut-off 0.05 Ua/ mL) at the age of 1 year was associated with early as well as late (i.e. between the age of 2 and 6 years) allergy development. Cord blood Foxp3/CD3γ mRNA ratios were significantly lower in early allergic children and levels below 0.32 predicted the allergic outcome. Conclusions and clinical Relevance Low cord blood Foxp3/CD3γ mRNA ratios are highly predictive for early allergy development, whereas specific IgE levels to hen's egg white above 0.05 Ua/ mL at age 1 year predict allergy development in general. [ABSTRACT FROM AUTHOR]

Cite this as: D. M. A. Bullens, Clinical & Experimental Allergy, 2010 (40) 958–961. [ABSTRACT FROM AUTHOR]

Background Staphylococcus aureus Enterotoxin B (SEB) has immunomodulatory effects in allergic airway disease. The potential contribution of SEB to the sensitization process to allergens remains obscure. Objective In order to study the effects of staphylococcal-derived toxins on the sensitization to ovalbumin (OVA) and induction of allergic airway inflammation, we have combined the nasal application of OVA with different toxins. Methods Nasal applications of OVA and saline, SEA, SEB, toxic shock syndrome toxin (TSST)-1, protein A or lipopolysaccharide (LPS) were performed on alternate days from day 0 till 12. On day 14, mice were killed for the evaluation of OVA-specific IgE, cytokine production by mediastinal lymph node (MLN) cells and bronchial hyperreactivity (BHR) to inhaled metacholine. The effect of SEB on dendritic cell (DC) migration and maturation, and on T cell proliferation was evaluated. Results Concomitant endonasal application of OVA and SEB resulted in OVA-specific IgE production, whereas this was not found with SEA, TSST-1, protein A, LPS or OVA alone. Increased DC maturation and migration to the draining lymph nodes were observed in OVA/SEB mice, as well as an increased T cell proliferation. Bronchial inflammation with an influx of eosinophils and lymphocytes was demonstrated in OVA/SEB mice, together with hyperresponsiveness and the production of IL-4, IL-5, IL-10 and IL-13 by MLN stimulated with OVA. Conclusions Our data demonstrate that SEB facilitates sensitization to OVA and consecutive bronchial inflammation with features of allergic asthma. This is likely due to augmentation of DC migration and maturation, as well as the allergen-specific T cell proliferation upon concomitant OVA and SEB application. Cite this as: W. Huvenne, I. Callebaut, M. Plantinga, J. A. J. Vanoirbeek, O. Krysko, D. M. A. Bullens, P.Gevaert, P. Van Cauwenberge, B. N. Lambrecht, J. L. Ceuppens, C. Bachert and P. W. Hellings, Clinical & Experimental Allergy, 2010 (40) 1079–1080. [ABSTRACT FROM AUTHOR]

Background The role of bacterial enterotoxins like Staphylococcus aureus enterotoxin B (SEB) in allergic asthma remains unknown. We used a mouse model of airway allergy to study the effects of nasal or bronchial contact with SEB on bronchial allergic inflammation. Methods The features of allergic asthma were induced in ovalbumin (OVA)-sensitized mice (days 1–13) by repeated exposures to nebulized OVA (days 33–37). Nasal or bronchial application of SEB was performed on three occasions (days 33–35–37), and the effects on bronchial inflammation, IgE titres and expression levels of mRNA for T helper type 2 cytokines and other inflammatory mediators were evaluated. Results Both nasal and bronchial SEB enhanced the allergen-induced bronchial inflammation, as reflected by more eosinophilic inflammation in the airway lumen and in bronchial tissue. Aggravation of experimental asthma correlated with higher expression of mRNA for IL-5, IL-4, IFN-γ, IL-12 p40, eotaxin-1 and TGF-β in bronchi. In addition, nasal SEB elevated concentrations of IL-4, IL-5 and IFN-γ in serum and bronchial SEB increased titres of OVA-specific and total IgE in serum. Conclusion Our data illustrate the potential of both nasal as well as bronchial SEB to aggravate several features of allergic asthma in a mouse model. [ABSTRACT FROM AUTHOR]

Background T-helper type 2 (Th2) cells play an important role in the pathogenesis of allergic diseases. Recent studies have demonstrated that allergen-specific T cells can also be found in the blood of healthy individuals. Both IL-10 and IFN-γ might modulate the induction and maintenance of allergen-specific tolerance. Aim To study the phenotype and functional characteristics of allergen-specific T cells in healthy non-atopic children. Methods Peripheral blood mononuclear cells (PBMC) from 13 symptomatic house dust mite (HDM)-allergic children and from nine matched healthy control children were stimulated with recombinant (r)Der p 2, a major allergen from HDMs. Results Stimulation with rDer p 2 resulted in Th2 cytokine production in cultures of PBMC from allergic but not from healthy children. In contrast, IL-10 and IFN-γ were induced in PBMC cultures from both healthy and HDM-allergic children. Intracellular staining revealed that IL-10 and IFN-γ are largely produced by the same T cells. Stimulation of T cells from healthy children with rDer p 2 also induced expression of inducible costimulator (ICOS) on a small T cell subset. Conclusion Allergen-specific memory T cells from healthy non-atopic children produce IL-10 and IFN-γ (but not Th2 cytokines) and express ICOS upon stimulation. These cells might be responsible for a normal immune balance after allergen encounter in non-atopics. [ABSTRACT FROM AUTHOR]

T helper (Th)2 cells play an important role in the development of IgE mediated diseases, with local overproduction of Th2 cytokines (IL-4. IL-5 and IL-13) at the site of allergic inflammation. Furthermore, IL-10 has been suggested to play a modulatory role in the induction and maintenance of allergen-specific tolerance in human atopic diseases. We studied whether circulating allergen-specific Th2 cells persist outside the season of exposure in patients mono-sensitized to birch pollen and whether healthy control individuals also have allergen specific Th2 cells. We also studied whether IL-10-producing allergen specific T cells can be found in circulation either in healthy controls or in allergic patients. Blood was drawn outside the birch-pollen season from 15 birch-pollen allergic patients. with seasonal respiratory symptoms and with (n = 12) or without (n = 3) oral allergy syndrome, and from 10 matched healthy controls. Peripheral blood mononuclear cells (PBMCs) were stimulated in vitro with recombinant Bet v I allergen, control antigen tetanus toxoid (TT) and anti-CD3 CD80. In part of the cultures, rIL-4 was added in order to reinforce the allergen specific Th2 cell responses. In the presence of rBet v I. T cells from allergic patients, but not from healthy controls. produced IL-4. IL-5 and IL-13. IL-5 production by patients T cells was further enhanced by adding more IL-4. In contrast, rBet v I together with IL-4-induced significant IL-10 production in control subjects but not in patients. Both Th1 and Th2 cytokines were equally induced by polyclonal stimulation in allergic patients and controls, but in the presence of IL-4. polyclonally induced IL-10 production was lower in the patient group. rBet v I specific Th2 cells circulate outside the season of exposure in the blood of birch pollen-allergic subjects but not in healthy controls. Allergen specific I cells were also demonstrated in controls hut these cells produce IL-10 when stimulated with rBet v I in the presence of IL-4. Our data reveal a different allergen induced cytokine profile in birch pollen allergic patients vs. controls. and suggest that a regulatory mechanism involving IL-4-induced allergen specific IL-10 production might be defective in allergic subjects. [ABSTRACT FROM AUTHOR]

The article presents a commentary on the search for T cells in allergic disorders. According to the author, different T-cell populations exist and their role in allergy is only partly revealed. The author adds that though allergic disorders are characterized by cellular infiltration and mediators, there are still obstacles that affect the search.