Nasal sensitization.

Abstract

Because humans breathe through the nose, the nasal mucosa becomes sensitized to inhalant allergens. Allergic rhinitis is, together with allergic conjunctivitis, the best example of a type I hypersensitivity reaction. It is an inflammation of the nasal mucosa induced by specific immune recognition of exogenous allergens. The production of IgE plays a major role in the pathophysiology. During the sensitization phase, an antigen is presented to an antigen-presenting cell at the epithelial level. Cells that express class II major histocompatibility complex Ia on their surface can act as an antigen-presenting cell for immunocompetent cells (dentritic cells, monocytes, macrophages, B lymphocytes and epithelial cells). Macrophages and Langerhans cells are increased in number in the nasal mucosa of patients with seasonal allergic rhinitis during the season and also after allergen challenge. Topical corticosteroid treatment reduces the number of Langerhans cells in the epithelium. The epithelium also participates in antigen presentation through its possession of antigen-binding surface proteins. The antigen is finally presented to CD4 T-helper cells and B cells; this is monitored by cytokines and leads to the development of memory cells and IgE-producing plasmocytes. In humans, IL-4 has been shown to be capable of differentiating B cells into IgE-producing plasma cells. The IL-4 production is inhibited by interferon gamma and by prostaglandin E2. The CD4+ cells also produce IL-2, which causes differentiation and proliferation of T lymphocytes, and IL-3, IL-5, IL-6 and IL-7, which stimulate the B lymphocytes. Topical administration of anti-allergic drugs or immunotherapy seems to be a logical approach in the treatment of patients with allergic rhinitis, because it has very direct activity on the main components of nasal sensitization.