Published online: October 25, 2016
Allergy to house dust mites contributes to chronic rhinitis and asthma in millions of children and adults worldwide, causing tremendous health and economic burden in high- and middle-income countries. The disease is caused by antibodies called immunoglobulin E (IgE). It starts in childhood and currently can be only controlled with symptomatic drugs, allergen avoidance, and specific immunotherapy. Therefore, primary and secondary prevention is a global research priority.
In a recent study published in The Journal of Allergy and Clinical Immunology (JACI) Posa and colleagues examined with innovative molecular methods and nanotechnologies the sera of over 700 German children whose blood had been repeatedly collected and symptoms constantly monitored between 1990 and 2010, i.e. from birth to age 20, to discover how allergy to mites starts and evolves and why some children develop more severe sensitization and symptoms than others.
The researchers described that mite allergy starts in children (often when they are still healthy) with an immune response to one or more of three molecules: Der p 1, Der p 2 and Der p 23 (group “A” molecules); some children, but not others, then proceed with an allergic “cascade” involving other molecules (Der p 4, 5, 7, and 21 = group “B”), and only a few children become sensitized also to Der p 11, 14, 15, and clone 16 (group “C”). This phenomenon is defined the “molecular spreading” or simply “the ABC” progression of mite allergy.
To have parents with allergic rhinitis, and a heavy exposure to mite allergens in early childhood are the strongest determinants of a strong progression (“ABC”) allergy to mites. Moreover, children starting their allergic sensitization before the third birthday have the strongest spreading of their allergic sensitization. Furthermore children with IgE sensitization to more molecules (stage “ABC” of allergic sensitization) are at higher risk of allergic rhinitis and asthma. Finally data show that the children sensitized already at pre-school age to Der p 1 or Der p 23, but not those sensitized only to Der p 2, have higher risk of having allergic asthma at school age.
The study demonstrates that subjects with IgE sensitization to more molecules (stage “ABC” of allergic sensitization) are at higher risk of allergic rhinitis and asthma. The Author suggests that these results may inspire predictive algorithms and prevention strategies against the progression of IgE sensitization to mites toward allergic rhinitis and asthma.
The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.