Increased expression of HLA-DR and CD86 in nasal epithelial cells in allergic rhinitics: antigen presentation to T cells and up-regulation by diesel exhaust particles

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A proportion of nasal epithelial cells (NEC) in patients with allergic rhinitis (AR) are known to express the major histocompatibility complex Class II molecule (HLA-DR).


We hypothesized that NEC may play a role in antigen presentation to T cells. To elucidate the possible role of NEC in antigen presentation, we examined the expression of HLA-DR, CD80 and CD86 in NEC, their regulation by cytokines and the capacity of NEC to induce antigen-specific proliferation of T cells.


We examined the expression of HLA-DR, CD80 and CD86 in nasal epithelial scrapings of patients with seasonal allergic rhinitis (SAR) to Japanese cedar pollen pre-season and in-season, by immunohistochemistry. Next, we examined the effect of IL-1β, TNF-α, (IFN-γ), IL-4 α, IL-13 and diesel exhaust particles (DEP) on the HLA-DR, CD80 and CD86 expression in cultured nasal epithelial cells (CNEC), by flow cytometry. Further, we analysed the capacity of mite antigen (Der f II)-pulsed mitomycin-C-treated CNEC to induce proliferation of autologous T cells from patients with perennial allergic rhinitis.


NEC constitutively expressed HLA-DR and CD86, but not CD80. The expression of HLA-DR and CD86 in NEC was significantly increased in-season, in patients with SAR as compared with that of pre-season. While IFN-γ up-regulated the expression of HLA-DR, IL-1β and TNF-α up-regulated the expression of CD86 in CNEC. Furthermore, in the presence of mite antigen, CNEC induced the proliferation of autologous peripheral blood T lymphocytes. Anti-CD86 and anti-HLA-DR monoclonal antibody but not anti-CD80 inhibited the epithelial cell-induced T cell proliferation. Stimulation with a combination of DEP and mite antigen significantly up-regulated HLA-DR and CD86 expression in CNEC.


These studies suggest that NEC in patients with AR may play a role in antigen presentation through the enhanced expression of HLA-DR and CD86. Furthermore, these results suggest the possibility that DEP may enhance the antigen-presenting function of CNEC.

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