Predominant Api m 10 sensitization as risk factor for treatment failure in honey bee venom immunotherapy

Frick, Marcel; Fischer, Jörg; Helbling, Arthur; Ruëff, Franziska; Wieczorek, Dorothea; Ollert, Markus; Pfützner, Wolfgang; Müller, Sabine; Huss-Marp, Johannes; Dorn, Britta; Biedermann, Tilo; Lidholm, Jonas; Ruecker, Gerta; Bantleon, Frank; Miehe, Michaela; Spillner, Edzard; Jakob, Thilo (2016). Predominant Api m 10 sensitization as risk factor for treatment failure in honey bee venom immunotherapy. Journal of allergy and clinical immunology, 138(6), 1663-1671.e9. Elsevier 10.1016/j.jaci.2016.04.024

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BACKGROUND

Component resolution recently identified distinct sensitization profiles in honey bee venom (HBV) allergy, some of which were dominated by specific IgE to Api m 3 and/or Api m 10, which have been reported to be underrepresented in therapeutic HBV preparations.

OBJECTIVE

We performed a retrospective analysis of component-resolved sensitization profiles in HBV-allergic patients and association with treatment outcome.

METHODS

HBV-allergic patients who had undergone controlled honey bee sting challenge after at least 6 months of HBV immunotherapy (n = 115) were included and classified as responder (n = 79) or treatment failure (n = 36) on the basis of absence or presence of systemic allergic reactions upon sting challenge. IgE reactivity to a panel of HBV allergens was analyzed in sera obtained before immunotherapy and before sting challenge.

RESULTS

No differences were observed between responders and nonresponders regarding levels of IgE sensitization to Api m 1, Api m 2, Api m 3, and Api m 5. In contrast, Api m 10 specific IgE was moderately but significantly increased in nonresponders. Predominant Api m 10 sensitization (>50% of specific IgE to HBV) was the best discriminator (specificity, 95%; sensitivity, 25%) with an odds ratio of 8.444 (2.127-33.53; P = .0013) for treatment failure. Some but not all therapeutic HBV preparations displayed a lack of Api m 10, whereas Api m 1 and Api m 3 immunoreactivity was comparable to that of crude HBV. In line with this, significant Api m 10 sIgG4 induction was observed only in those patients who were treated with HBV in which Api m 10 was detectable.

CONCLUSIONS

Component-resolved sensitization profiles in HBV allergy suggest predominant IgE sensitization to Api m 10 as a risk factor for treatment failure in HBV immunotherapy.

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