Allergen-component Diagnostics Food-pollen Allergy
We are encouraged to utilize allergen-component diagnostics for food-pollen allergy in order to guide advice. But these tests are expensive in our country. What is the minimum test profile you would recommend to identify PR-10, profilin, and LTP components. For example, would Pru p 1,3 and 4 be sufficient?
By Professor Wayne Thomas
Allergic sensitivity to rosaceous fruits in the Mediterranean region shows an interesting and clinically useful pattern when the IgE binding is measured by component resolved diagnosis (1, 2). Sensitisation to the non-specific lipid transfer protein (LTP) from peach, Pru p 3, is associated with a higher likelihood that subjects will experience systemic symptoms and not just oral allergy symptoms and in addition allergic symptoms from ingesting other fruits and vegetables. These not only include other rosaceous fruits but a long list of genetically disparate plants including celery, carrot, walnut, fennel, peanut, cereals and tomato. The LTP sensitisation is not only best measured with Pru p 3 but it appears that the sensitisation is driven by peach allergen. Sensitisation to the PR-10-like proteins (Bet v 1 homologues) and profilins without LTP is associated with oral allergy syndrome and not systemic reactions and curiously subjects co-sensitised with these specificities and LTP are have fewer symptoms than those sensitised to LTP alone (3). Knowledge that LTP is usually found in the peal of the fruit and vegetable and that profilin sensitisation is associated with melon allergy provides further assistance with the clinical management. There are additional associations of symptoms with sensitisation to the aeroallergen LTPs of the mugwort and plane-tree pollens with the risk of more severe allergy (4) and LTP induced rhinitis (5). This again appears to dependent on the primary peach sensitization because higher IgE titres are found to Pru p 3 (5) and is not found for pollens with the evolutionary more disparate LTP sequences like those found in olive, Parieteria spp. and ragweed pollens. With respect to diagnostic/prognostics tests within the Mediterranean region, Pru p 3 is the LTP of choice. Also within this region profilins from disparate pollen sources have essentially the same IgE binding for subjects sensitised by different species even for subjects selected for peach allergy (6). Grass (Phl p 12), birch (Bet v 2) and date palm (Pho d 2) all appear suitable and a large study of pan allergens (7) showed a good association of titres to diverse pollen profilins. The PR-10 proteins do not exhibit the same concordance of cross reactivity amongst diverse species and allergen source (7) and indeed the food and pollen PR-10 can be divided into food and pollen groups. Mal d 1 from apple detects anti-PR-10 antibodies in fruit allergic subjects better than Bet v 1(8) although in Europe titres of Bet v 1-reactive antibodies are high with pollen sensitisation plus LTP allergy. Sensitisation to Mal d 1 could be used measure PR-10 sensitisation to the food group and Bet v 1 for pollen sensitisation, although they do cross-react. From published reports Pru a 1 and 4 would probably be suitable for PR-10 food markers and profilin but have not been as extensively used.
The findings above have not been ascertained outside of the Mediterranean region and there are reports to show that they do not necessarily apply. LTP sensitisation of hazelnut-allergic children living in northern Europe have IgE reactivity to Cor a 8, the hazelnut LTP, but not to Pru p 3 (9). In the geographically more distant northern China there is an association of mugwort sensitisation and peach allergy but in contrast to the Mediterranean allergy it is driven by IgE produced to the mugwort Art v 3 with little reactivity to Pru p 3 (10). It follows that Pru p 3 would not be suitable for diagnosis in China although the clinical spectrum of the LTP sensitisation has not been studied to the same degree in this region. A smaller group with LTP peach allergy with no association or sensitisation to mugwort was also found (10).
- Egger M. Hauser M. Mari A. Ferreira F. Gadermaier G. The role of lipid transfer proteins in allergic diseases. Current Allergy & Asthma Reports. 10(5):326-35, 2010
- Asero R. Pravettoni V. Anaphylaxis to plant-foods and pollen allergens in patients with lipid transfer protein syndrome. Current Opinion in Allergy & Clinical Immunology. 13(4):379-85, 2013
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- Pascal M. Munoz-Cano R. Reina Z. Palacin A. Vilella R. Picado C. Juan M. Sanchez-Lopez J. Rueda M. Salcedo G. Valero A. Yague J. Bartra J. Lipid transfer protein syndrome: clinical pattern, cofactor effect and profile of molecular sensitization to plant-foods and pollens. Clinical & Experimental Allergy. 42(10):1529-39, 2012
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- Pastorello EA. Farioli L. Stafylaraki C. Mascheri A. Scibilia J. Pravettoni V. Primavesi L. Piantanida M. Nichelatti M. Asero R. Anti-rPru p 3 IgE levels are inversely related to the age at onset of peach-induced severe symptoms reported by peach-allergic adults. International Archives of Allergy & Immunology. 162(1):45-9, 2013.
- Scala E. Alessandri C. Palazzo P. Pomponi D. Liso M. Bernardi ML. Ferrara R. Zennaro D. Santoro M. Rasi C. Mari A. IgE recognition patterns of profilin, PR-10, and tropomyosin panallergens tested in 3,113 allergic patients by allergen microarray-based technology. PLoS ONE [Electronic Resource]. 6(9):e24912, 2011.
- Vieira T. Cunha L. Neves E. Falcao H. Diagnostic usefulness of component-resolved diagnosis by skin prick tests and specific IgE to single allergen components in children with allergy to fruits and vegetables. Allergologia et Immunopathologia. 42(2):127-35, 2014
- Flinterman AE, Akkerdaas JH, den Hartog Jager CF, et al. Lipid transfer protein-linked hazelnut allergy in children from a non-Mediterranean birch-endemic area. Journal of Allergy & Clinical Immunology 121:423–28, 2008
- Gao ZS. Yang ZW. Wu SD. Wang HY. Liu ML. Mao WL. Wang J. Gadermaier G. Ferreira F. Zheng M. van Ree R. Peach allergy in China: a dominant role for mugwort pollen lipid transfer protein as a primary sensitizer. Journal of Allergy & Clinical Immunology. 131:224-6, 2013
Wayne Thomas, PhD
Division of Molecular Biotechnology
Telethon Institute for Child Health Research
West Perth, Australia