BACKGROUND: B7 molecules (CD80, CD86) and their counter-receptors, CD28 and CD152 (CTLA-4), play an important role in T cell-mediated immune responses. We previously demonstrated that B7 molecules are selectively up-regulated not only on B cells but also on T cells from the peripheral blood mononuclear cells of patients with perennial rhinitis cultured with allergen. However, the expression of CD80/CD86 molecules and their counter-receptors in nasal mucosa, the actual inflammatory site of allergic rhinitis, has not yet been clarified. PATIENTS AND METHODS: Inferior turbinates from patients with either allergy to house dust or non-allergic rhinitis were excised and immunohistologically stained. In addition, the inferior turbinates were challenged with paper discs containing extracts of house dust and subsequently excised. Samples were double stained with immunofluorescent-labelled antibody to identify cells bearing CD86. RESULTS: Without the nasal provocation, only the expression of CD86 was increased in nasal mucosa of patients with allergic rhinitis compared with those with non-allergic rhinitis. However, following the nasal provocation with house dust, not only CD86, but also CD80, CD28, and CD152 were significantly expressed in allergic patients. Immunofluorescent double staining revealed CD86 expression in CD19, CD1a, CD14 and CD3 lymphocytes. CONCLUSION: These results indicate that the expression of CD80/CD86 molecules and their counter-receptors is induced in allergic patients following nasal provocation with allergen, suggesting a local amplification of allergen-specific immune responses in perennial rhinitis.
BACKGROUND: B7 molecules (CD80, CD86) and their counter-receptors, CD28 and CD152 (CTLA-4), play an important role in T cell-mediated immune responses. We previously demonstrated that B7 molecules are selectively up-regulated not only on B cells but also on T cells from the peripheral blood mononuclear cells of patients with perennial rhinitis cultured with allergen. However, the expression of CD80/CD86 molecules and their counter-receptors in nasal mucosa, the actual inflammatory site of allergic rhinitis, has not yet been clarified. PATIENTS AND METHODS: Inferior turbinates from patients with either allergy to house dust or non-allergic rhinitis were excised and immunohistologically stained. In addition, the inferior turbinates were challenged with paper discs containing extracts of house dust and subsequently excised. Samples were double stained with immunofluorescent-labelled antibody to identify cells bearing CD86. RESULTS: Without the nasal provocation, only the expression of CD86 was increased in nasal mucosa of patients with allergic rhinitis compared with those with non-allergic rhinitis. However, following the nasal provocation with house dust, not only CD86, but also CD80, CD28, and CD152 were significantly expressed in allergicpatients. Immunofluorescent double staining revealed CD86 expression in CD19, CD1a, CD14 and CD3 lymphocytes. CONCLUSION: These results indicate that the expression of CD80/CD86 molecules and their counter-receptors is induced in allergicpatients following nasal provocation with allergen, suggesting a local amplification of allergen-specific immune responses in perennial rhinitis.