CRD: Monitoring of allergy progression
Birth cohort studies have shown a sequential broadening of the IgE response to complex allergen sources. The IgE response starts in general with a monomolecular stage and then, through an oligomolecular sensitization pattern becomes polymolecular30. This “molecular spreading” has been observed in many participants in the MAS birth cohort allergic to Timothy grass. In this case, the “initiator molecule” was Phl p 1. However, only a few patients develop an extremely polymolecular response, producing IgE antibodies to all the best known allergenic molecules of Phleum pratense (Phl p 1, Phl p 2, Phl p 4, Phl p 5, Phl p 6, Phl p 7, Phl p 11 and Phl p 12)30. Similarly, molecular spreading has been observed in the MAS cohort among children developing IgE sensitization against Dermatophagoides pteronyssinus 31. In this case, multiple “initiator molecules” have been observed (Der p 1, Der p 2, Der p 23). In these children, sensitization started with Der p 1 and/or Der p 2 and/or Der p 23 (defined as group “A” molecules); then involved Der p 4, Der p 5, Der p 7, and Der p 21 (group “B” molecules); and was completed with IgE to Der p 11, Der p 14, Der p 15, Der p 18, and clone 16 (group “C” molecules). This expansion of the IgE response has also been defined as “the ABC march” of mite allergy31. Children with a broader polymolecular IgE sensitization pattern were also more frequently affected by asthma when compared with those who remained in the “A” stage of IgE sensitization31. A similar trend was observed among grass pollen allergic children in the Manchester Allergy and Asthma Study (MAAS)32. In this case, children with broader molecular patterns of IgE sensitization had also a significantly increased risk for asthma, eczema, and rhinitis32. It has also been proposed that earlier administration of AIT, i.e. at a mono- or oligomolecular stage of sensitization, may be more effective than at later stages 33.