Antigen presenting cells in the nasal mucosa of patients with allergic rhinitis during allergen provocation

Abstract

Background: The role of antigen presenting cells (APC) in allergic rhinitis is underexposed. Allergen presentation to T lymphocytes is probably an important aspect of the pathophysiological mechanism of allergic rhinitis.

Objectives: The aim of the study was to investigate the presence and dynamics of APC with special emphasis on Langerhans cells (LC) in the nasal mucosa of patients with an isolated grass pollen allergy during an out-of-season 2-week allergen exposure, mimicking the natural grass pollen season.

Methods: Seventeen patients with isolated grass pollen allergy and four control subjects were challenged daily with allergen during a 2-week period in the winter. Biopsy specimens were obtained once before, six times during and once after the provocation period. Biopsy sections were stained with monoclonal antibodies: OKT6 (CD1a-Langerhans cells), Ki-M6 (CD68-macrophages), L25 (dendritic cells), anti-IgE, HLA-DR and HLA-DQ (Major Histocompatibility Complex Class II-antigen presenting cells), as well as staining with acid phosphatase.

Results: APC with different characteristics are present in the epithelium and lamina propria of the nasal mucosa. The number of LC increased significantly in epithelium and lamina propria. IgE(+)-LC were present in the nasal mucosa and increase during provocation. HLA-DR+ cells with dendritic and lymphocytic morphology and HLA-DQ+ cells were found. The number of these cells increased during provocation in epithelium and lamina propria. The number of HLA-DR+ epithelial cells did not change. A significant increase in the number of Ki-M6+ cells (macrophages) was found in the lamina propria. However, Ki-M6+ cells increased to the same extent in the lamina propria in the control group.

Conclusion: APC are influenced by allergen provocation. This study supports the hypothesis that (IgE+) LC are involved in allergic rhinitis. The role macrophages play remains doubtful.