Detection of ovomucoid‐specific low‐affinity IgE in infants and its relationship to eczema

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Immunoglobulin E (IgE) plays key roles in type I hypersensitivity in allergic individuals. Two distinct pathways of IgE class switching have been proposed in mice: a sequential class switching pathway (μ → γ → ε), which can generate high‐affinity IgE through somatic hypermutation at IgG1, and a direct class switching pathway (μ → ε), which can generate low‐affinity IgE 1.
Assessment of the immunologic changes that occur during the first year of life is important for understanding the mechanisms of allergen sensitization and allergy development in humans. We previously reported a highly sensitive allergen microarray on a densely carboxylated protein (DCP) chip 2, and this method has been validated in successive studies 4. Using the DCP chip method, we identified a food allergen‐specific IgE (sIgE) with low‐affinity characteristics in cord blood (CB) that had no cross‐reactivity to other immunoglobulins 4 and induced an insufficient IgE response in a luciferase‐reporting mast cell line, RS‐ATL8 cells 5.
Antigens, such as hen's egg proteins, seem to be transferred to the fetus/infant through placenta, breast milk, baby food, or disrupted skin. In this study, we detected low‐affinity ovomucoid (OM)‐sIgE in cord blood and during infancy. We also investigated the relationship between low‐/high‐affinity IgE antibodies and the risk factors for allergic sensitization during infancy, such as feeding, eczema, and solid food consumption.

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