Research
Specific IgE response to different grass pollen allergen components in children undergoing sublingual immunotherapy
1 Spin-Off ATRP Srl, Allergic Tests Research and Production, Perugia, Italy
2 Allergy/Pulmonary rehabilitation, ICP Hospital, Milan, Italy
3 Medical and Scientific Department, Stallergenes, Milan, Italy
4 Institute of Pediatrics, Department of Medical and Surgical specialty and Public Health, Perugia, Italy
Clinical and Molecular Allergy 2012, 10:7 doi:10.1186/1476-7961-10-7
Published: 13 June 2012Abstract
Background
Grass pollen is a major cause of respiratory allergy worldwide and contain a number of allergens, some of theme (Phl p 1, Phl p 2, Phl p 5, and Phl 6 from Phleum pratense, and their homologous in other grasses) are known as major allergens. The administration of grass pollen extracts by immunotherapy generally induces an initial rise in specific immunoglobulin E (sIgE) production followed by a progressive decline during the treatment. Some studies reported that immunotherapy is able to induce a de novo sensitisation to allergen component previously unrecognized.
Methods
We investigated in 30 children (19 males and 11 females, mean age 11.3 years), 19 treated with sublingual immunotherapy (SLIT) by a 5-grass extract and 11 untreated, the sIgE and sIgG4 response to the different allergen components.
Results
Significant increases (p < 0.001) were detected for Phl p 1, Phl p 2, Phl p 5, and Phl p 6, while sIgE levels induced in response to Phl p 7 and Phl p 12 were low or absent at baseline and unchanged following SLIT treatment; no new sensitisation was detected. As to IgG4, significant increases were found for Phl p2 and Phl p 5, while the increase for Phl p 12 was not significant. In the control group, no significant increase in sIgE for any single allergen component was found.
Conclusions
These findings confirm that the initial phase of SLIT with a grass pollen extract enhances the sIgE synthesis and show that the sIgE response concerns the same allergen components which induce IgE reactivity during natural exposure.



