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.
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-1beta, TNF-alpha, (IFN-gamma), IL-4 alpha, 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-gamma up-regulated the expression of HLA-DR, IL-1beta and TNF-alpha 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.
Takizawa
R
R
Department of Otolaryngology, Nippon Medical School, Tokyo, Japan.
Pawankar
R
R
Yamagishi
S
S
Takenaka
H
H
Yagi
T
T
D000328:Adult; D017951:Antigen Presentation; D000938:Antigen-Presenting Cells; D051940:B7-2 Antigen / Q000276:immunology*; D004847:Epithelial Cells / Q000276:immunology*; D006684:HLA-DR Antigens / Q000276:immunology*; D006801:Humans; D007564:Japan; D008297:Male; D009297:Nasal Mucosa / Q000276:immunology*; D012220:Rhinitis / Q000276:immunology*; D015854:Up-Regulation / Q000276:immunology; D001335:Vehicle Emissions / Q000633:toxicity*
D051940:B7-2 Antigen; D006684:HLA-DR Antigens; D001335:Vehicle Emissions