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.