Background: We measured specific IgE levels against the recombinant allergens (RAs) rPhl p 1, rPhl p 2, rPhl p 5 in patients allergic to grass pollen, and examined the existence of different patterns of IgE production to RAs. The seasonal variations of IgE levels to rPhl p 1, rPhl p 2, and rPhl p 5 were considered, too.
Methods: Blood was taken from 276 consecutive patients with allergy to grass pollen diagnosed by patient history and skin prick testing. Total and specific serum IgE was measured by the immunoenzymatic CAP FEIA System. Eosinophil cationic protein (ECP) and myeloperoxidase (MPO) were assessed by radioimmunoassay according to the instructions of the manufacturers.
Results: We observed eight different patterns of IgE production to rPhl p 1, rPhl p 2, and rPhl p 5 in patients with specific IgE to timothy grass. A significant difference between the values of IgE levels to timothy and the sum of each level of specific IgE to individual RAs was found (P=0.039, Wilcoxon matched pairs test) in the whole population (n=276 subjects). In four subgroups of patients, the sum of each level of specific IgE to individual RAs was equal to the levels of specific IgE to timothy grass extract. In one subgroup, the sum of IgE to RAs was lower than the levels of IgE to the natural counterpart (P=0.013). A lack of subjects in two subgroups did not permit comparison at all. Finally, three subjects with specific IgE to timothy did not show specific IgE to RAs. Out of 276 patients, blood was taken from two different groups of subjects at different time points: November–January and May–July, respectively. The median values were as follows: total IgE=139 kU/l, IgE to timothy=10.2 kUA/l; IgE to rPhl p 1=3.6 kUA/l, to rPhl p 2=<0.35 kUA/l, and to rPhl p 5=1.1 kUA/l; ECP=8.2 g/l; MPO=303 g/l (before exposure to grass pollen); total IgE=159 kU/l, IgE to timothy=57.2 kUA/l; IgE to rPhl p 1=22.1 kUA/l, to rPhl p 2=5.9 kUA/l, and to rPhl p 5=3.9 kUA/l; ECP=16.2/l, MPO=413.0/l (during the pollen season). There were significant variations of specific IgE levels between the patients exposed to pollen and the unexposed patients. Moreover, there were statistical differences in the IgE and inflammation mediator levels in sera from the pre-to the pollen season (P<0.02).
Conclusions: The results suggest that RAs allow establishment of the patient's IgE-reactivity profile, encourage future research, and encourage manufacturers to produce further RAs for precise diagnosis and substantially improved immunotherapy injection of only those allergens against which significant amounts of specific IgE are produced.