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    • br Immune profile of food allergy Despite the fact that

    2018-11-14


    Immune profile of food allergy Despite the fact that IgE plays a central role in the pathogenesis of food allergy, measurement of food-specific IgE is not diagnostic in isolation. Quantification of food-specific IgE antibody levels in serum can identify patients in the pediatric population who are highly likely (>95%) to experience clinical reactions to egg, milk, peanut or fish, as recently reviewed (Chokshi and Sicherer, 2016). However lower levels poorly discriminate between those who are sensitized versus allergic. Detection of IgE reactivity against components of food (for example the protein allergen Ara h 2 in peanut or Cor a 14 for hazelnut) improves specificity (Klemans et al., 2015; Beyer et al., 2015; Eller and Bindslev-Jensen, 2013). Ara h 2 is digestion-resistant and can trigger systemic reactions while Ara h 8 is cross-reactive with birch pollen fda approved (and can result in positive IgE to peanut in birch pollen-allergic individuals), is susceptible to digestion, and does not trigger systemic reactions. IgE levels against whole peanut extract would not discriminate between IgE to these two allergens with differing potential to trigger reactions. Antibody isotypes other than IgE, such as IgG and IgA, are not predictive of food allergy. However, ratio of egg white allergen-specific IgE/IgG4 has been shown to be better than IgE levels alone in predicting clinical reactivity to egg (Okamoto et al., 2012; Caubet et al., 2012). For the production of IgE antibodies, B cells require help from allergen-specific T cells producing IL-4, either Th2 or T follicular helper (Tfh) cells. T cells from allergic patients display a uniquely Th2 cytokine production profile (Prussin et al., 2009). IL-9 production from a T cell subset distinct from those producing IL-5 was recently reported to differentiate between children with peanut allergy and children with peanut sensitization (Brough et al., 2014). In addition, it was recently reported in mice that a population of intestinal mast cells express IL-9, promote experimental food allergy in an IL-9-dependent manner, and are dependent on Th2 cells for their development (Chen et al., 2015). Furthermore, the authors showed that in patients with food allergy, duodenal biopsies had elevated expression of genes associated with the mast cell signature (IL-9, IL-13, chymase, and tryptase). Thus innate events in the intestinal tissue may be critical for linking systemic Th2-skewed adaptive responses to symptoms. Food allergy is commonly referred to as a failure of oral tolerance, a systemic state of antigen-specific immune suppression that is mediated by regulatory T cells. However, there is little information on the role of Tregs in food allergy. In mouse models, administration of Tregs can suppress food allergy (Burton et al., 2014). Furthermore, in mice genetically susceptible to food allergy there is an impairment of Treg function, and evidence of Th2 reprogramming such that Tregs contribute to Th2 cytokine production rather than suppress it (Noval Rivas et al., 2015). This was also observed in peripheral blood of subjects with milk allergy (Noval Rivas et al., 2015), supporting the hypothesis that food allergy is a failure of regulatory T cells.
    Emerging evidence for the role of the skin in food allergy There is growing evidence pointing to the skin as the main site of sensitization to food allergens, particularly peanut. The majority of patients with peanut or tree nut allergy experienced their first reaction the first time that the food was knowingly ingested, so previous sensitization to the allergen has been proposed to occur in utero, through breast-milk, or by another route of exposure, such as topical exposure. Ezcema is a risk factor that strongly associated with food allergies (Martin et al., 2015). Infants presenting with eczema were 11 times more likely to present peanut allergy and 6 times more likely to have egg allergy, suggesting that alteration of the skin barrier facilitates contact with the allergen. Moreover, mutations in filaggrin, a protein essential to maintain skin barrier, have been associated with increased risk of food allergy (Brown et al., 2011).