Why lipid transfer protein allergy is not a pollen-food syndrome: novel data and literature review

¹Allergology Unit, Clinica San Carlo, Paderno Dugnano, Italy
²U.O.C. of Pathology Clinic, Ospedale Buccheri La Ferla F.B.F., Palermo, Italy
³SOS Allergy and Clinical Immunology, USL Toscana Centro, Prato, Italy
⁴Allergy and Immunology Unit, Istituti Clinici Scientifici Maugeri, IRCCS, Pavia, Italy
⁵UOC General Medicine Immunology and Allergology, IRCCS Foudation Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
⁶Clinical and Laboratory Molecular Allergy Unit, Istituto Dermopatico dell'Immacolata, Rome, Italy
⁷Centro Malattie Allergiche Prof. Giovanni Bonsignore, Istituto per la Ricerca e l'Innovazione Biomedica, CNR, Palermo, Italy
⁸SSD of Immunology and Allergology, Presidio Ospedaliero S. Maria degli Angeli, Pordenone, Italy

Summary
Background. Based on the cross-reactivity between pollen lipid transfer proteins (LTPs) and the peach LTP, Pru p 3, it has been suggested that the pollen might initiate the LTP sensitization process. Objective. To establish whether LTP allergy can be considered as a pollen-food syndrome. Methods. The literature was reviewed and new data of component-resolved diagnosis from Italy obtained by both ISAC immunoassay and ImmunoCAP on large populations of LTP hypersensitive patients were provided and analyzed. Results. Among Pru p 3 reactors, patients positive for Art v 3 and Pla a 3 largely exceeded those sensitized to the respective major pollen allergens, Art v 1 and Pla a 1/Pla a 2. Pru p 3 reactivity remained stable around 80-90% at all ages, whereas Art v 3 and Ole e 7 recognition was missing in younger patients. Pru p 3 IgE exceeded IgE specific for pollen LTP at all ages. Inhibition studies carried out on LTP reactors showed that commercial extracts of mugwort and plane pollen were unable to inhibit significantly Pru p 3 IgE reactivity. In follow-up studies, baseline Pru p 3 IgE levels exceeded Art v 3 IgE levels in 84% of those sensitized to both allergens, and all patients positive to only one LTP allergen at baseline were sensitized to Pru p 3. Further, most of the patients who did not show any LTP reactivity at baseline became exclusive Pru p 3 reactors. On ImmunoCAP singleplex Pru p 3 IgE levels exceeded Art v 3 IgE levels in 89% of cases (p < 0.0001). Most literature data were in keeping with these new observations. Conclusions. The evidence for LTP syndrome being a pollen-food syndrome is presently very thin. Our data do not rule out the possible sensitization to the protein, via the airways or the skin.