Background Currently, no estimates can be made on the impact of hematopoietic stem cell transplantation on allergy transfer or cure of the disease. By using component‐resolved diagnosis, we prospectively investigated 50 donor‐recipient pairs undergoing allogeneic stem cell transplantation. This allowed calculating the rate of transfer or maintenance of allergen‐specific responses in the context of stem cell transplantation. Methods Allergen‐specific IgE and IgG to 156 allergens was measured pretransplantation in 50 donors and recipients and at 6, 12 and 24 months in recipients post‐transplantation by allergen microarray. Based on a mixed effects model, we determined risks of transfer of allergen‐specific IgE or IgG responses 24 months post‐transplantation. Results After undergoing stem cell transplantation, 94% of allergen‐specific IgE responses were lost. Two years post‐transplantation, recipients' allergen‐specific IgE was significantly linked to the pretransplantation donor or recipient status. The estimated risk to transfer and maintain individual IgE responses to allergens by stem cell transplantation was 1.7% and 2.3%, respectively. Allergen‐specific IgG, which served as a surrogate marker of maintaining protective IgG responses, was highly associated with the donor's (31.6%) or the recipient's (28%) pretransplantation response. Conclusion Hematopoietic stem cell transplantation profoundly reduces allergen‐specific IgE responses but also comes with a considerable risk to transfer allergen‐specific immune responses. These findings facilitate clinical decision‐making regarding allergic diseases in the context of hematopoietic stem cell transplantation. In addition, it provides prospective data to estimate the risk of transmitting allergen‐specific responses via hematopoietic stem cell transplantation.

A lack of correlation between systemic and local IgE production at mucosal sites has been reported for allergic asthma [1–5], allergic rhinitis [6, 7] and chronic rhinosinusitis with nasal polyps [8–10]. In allergic asthmatics, local IgE production is higher than in nonallergic asthmatics [3] and high local IgE levels have been linked to the clinical phenotype. Interestingly, in cases of nasal polyps, local IgE targets mainly superantigens [8].