Immune Cell Characterization of Human Fungiform Papillae

Objectives: Clinical taste deficits are rare in the general population but are prevalent in 90% of head and neck cancer patients who receive radiation therapy. These patients experience substantial taste loss and alterations of food flavor perception which contribute to impaired food intake, malnutrition and failure to survive. While taste cells are capable of replacement throughout life, recovery following extensive damage to the lingual epithelium can require months and even years of regeneration. Radiation therapy may chronically alter the gustatory epithelia via repeated inflammatory insult, leading to subsequent histopathological changes and genetic alteration of the epithelial/gustatory regenerative cellular processes.

Methods: As an initial step in understanding the impact of lingual inflammation, we identified and determined the density of different immune cells in normal human fungiform papillae. Fungiform papillae from three healthy subjects (40-50 yrs old) were examined immunohistochemically for dendritic cells, macrophages, and lymphocytes.

Results: Among innate immune cells, CD11c+ dendritic cells were more prevalent than CD64+ macrophages, while the density of mature (CD83+) and immature (CD209+) dendritic cells were similar. T lymphocytes, identified with CD3, CD4, and CD8, were more prevalent than CD19+ B lymphocytes, and among T lymphocytes, CCR5+ Th1 cells were more prevalent than CCR4+ Th2 cells.

Conclusions: The immune cell profile plays a critical role in the barrier function of the oral mucosa and these data form the foundation for the study of taste loss subsequent to head and neck cancer in patients who receive radiation therapy to gustatory receptor fields. Correlation of cellular changes with perceptions of taste loss may help define subclinical taste abnormalities which influence the clinical course of therapy and assist in the identification of efforts to refine therapeutic interventions for patients with taste loss.

Support: NIH DC00214.