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

Takizawa, R.; Pawankar, R.; Yamagishi, S.; Takenaka, H.; Yagi, T.

Background 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). Objective 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. Methods 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. Results 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. Conclusions 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.