The present data demonstrate that parasympathetic activity has the capacity to activate dendritic cells to release OX40 ligand, the latter induces CD4+ T cells to produce IL-4 and TNF-alpha that may further contribute to the pathogenesis of NP.

The components of immune tolerance machinery, TolDCs and Tregs were suppressed in the AR nasal mucosa. The increases in SEB and decreases in avb6 in nasal epithelium are associated with the compromises of immune tolerance in the nasal mucosa. SEB has the ability to suppress the expression of avb6 in nasal epithelial cells.

CD98 plays a critical role in compromising the airway epithelial barrier function that contributes to the induction of airway allergy.

This paper reports the effects of the H2 antagonist cimetidine on the number of CD4+ and CD8+ cells in nasal mucosa and the IgE level of nasal secretions in patients with allergic rhinitis. The results showed the numbers of CD4+ cells were greater than the numbers of CD8+ cells in nasal mucosa, both in the patients with allergic rhinitis and normal subjects, but the ratio of CD4+:CD8+ cells was much higher in the patients with allergic rhinitis. After treatment with cimetidine locally for 4 weeks, the numbers of CD4+ cells fell and the numbers of CD8+ cells increased in the patients with allergic rhinitis. The high IgE level of nasal secretion of the patients with allergic rhinitis was much reduced after treatment with cimetidine. The results suggest that there are high numbers of CD4+ cells and lower numbers of CD8+ cells in the nasal mucosa and a high level of IgE in the nasal secretions of the patients with allergic rhinitis. Treatment with cimetidine locally may be of some value to relieve the clinical symptoms of allergic rhinitis.