Immunological aspects of allergy and anaphylaxis part 41




Recent research into the underlying immunological mechanisms of rhinitis has borne new insight into the pathophysiology of allergic rhinitis. Prior understanding favored initial IgE production in regional lymph nodes or bone marrow. Failure of prior experiments to co-localize IgE protein within B cells to the local tissue environment weighed heavily against localized tissue IgE production. In the past ten years, however, a growing body of research has challenged the former dogma that IgE production occured remotely from the allergen-tissue interface. Studies of local messenger RNA (mRNA) support the hypothesis of local protein synthesis. Durham and colleagues, using a combination of insitu hybridization and immunohistochemistry, showed that cells expressing epsilon-heavy chain mRNA (Cε) were present in the nasal mucosa of allergic individuals, and marked increases of these cells occured on exposure to allergen. Furthermore, the increases seen in IgE and Cε mRNA after allergen challenge were inhibited by topical corticosteroids, favoring a localized process. In addition, Kleinjan and colleagues used similar techniques to demonstrate finally IgE-producing B cells in the nasal mucosa. Biopsies were obtained from normal subjects and from seasonal and perennial subjects during pollen season and during house dust exposure. The study found no differences in B-cell numbers, either CD19 (B cells) or CD138 (immunoglobulin-secreting plasma cells) in allergic and normal patients. Allergic patients, however, exhibited  significantly greater numbers of IgE-positive B cells than normal patients, and allergen-positive cells were only found  in allergics with almost all such cells staining positive for IgE or CD138. The combination of these factors suggests local IgE production may take place in the mucosa during natural allergen exposure

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