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  • Mascarell, L., et al. (författare)
  • Characterization of oral immune cells in birch pollen-allergic patients: impact of the oral allergy syndrome and sublingual allergen immunotherapy on antigen-presenting cells
  • 2015
  • Ingår i: Allergy. - : Wiley. - 0105-4538. ; 70:4, s. 408-419
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: A detailed characterization of human oral immune cells is needed to better understand local mechanisms associated with allergen capture following oral exposure. Methods: Oral immune cells were characterized by immunohistology and immunofluorescence in biopsies obtained from three healthy individuals and 23 birch pollen-allergic patients with/without oral allergy syndrome (OAS), at baseline and after 5 months of sublingual allergen immunotherapy (AIT). Results: Similar cell subsets (i.e., dendritic cells, mast cells, and T lymphocytes) were detected in oral tissues from healthy and birch pollen-allergic individuals. CD207(+) Langerhans cells (LCs) and CD11c(+) myeloid dendritic cells (DCs) were found in both the epithelium and the papillary layer of the Lamina propria (LP), whereas CD68(+) macrophages, CD117(+) mast cells, and CD4(+)/CD8(+) T cells were rather located in both the papillary and reticular layers of the LP. Patterns of oral immune cells were identical in patients with/without OAS, except lower numbers of CD207(+) LCs found in oral tissues from patients with OAS, when compared to OAS(-) patients (P < 0.05). A 5-month sublingual AIT had a limited impact on oral immune cells, with only a significant increase in IgE(+) cells in patients from the active group. Colocalization experiments confirmed that such IgE-expressing cells mostly encompass CD68(+) macrophages located in the LP, and to a lesser extent CD207(+) LCs in the epithelium. Conclusion: Two cell subsets contribute to antigen/allergen uptake in human oral tissues, including (i) CD207(+) LCs possibly involved in the physiopathology of OAS and (ii) CD68(+) macrophages likely critical in allergen capture via IgE-facilitated mechanisms during sublingual AIT.
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