Bronchial asthma is characterized by episodic reversible narrowing of the airway, with associated bronchial hyperreactivity. Recent evidence indicates a possible role of activating T cells in the pathogenesis of asthma. The presence of activated T cells has been demonstrated in blood, bronchial biopsy specimens, and bronchoalveolar lavage fluid from asthmatics.
T cells may orchestrate inflammatory responses to inhaled antigen and other stimuli in asthma by producing several cytokines with widely varying features. Soluble interleukin-2 receptor (sIL-2R), a subunit of the IL-2 cell surface receptor, is secreted from cell membranes during T-cell activation and is a major parameter of T-cell activation. In patients with severe asthma as well as other diseases, increased serum sIL-2R has been documented. canadian health mall
In atopic-allergic asthma, specific T-cell clones exposed to antigen stimulate В cells to produce specific IgE. IgE, once fixed on mast cells and basophils, can trigger mediator release following cross-linking by an antigen. As one mechanism for IgE production, the addition of interleukin 4 (IL-4) at a determined period of culture is known to induce the production of IgE by В cells in a dose-dependent manner. In contrast, the interferon gamma (IFN-y) antagonized IL-4 effect on В cells inhibits IgE production. These two factors possibly interact in vivo to bring about IgE production.
Soluble Fc epsilon receptor II (FceRII) is a soluble fragment of FceRII expressed mainly on В cells. FceRII is poorly expressed on normal В cells but its expression is enhanced by IL-4. Interferon gamma inhibits the effect of IL-4 on FceRII expression. IgE production and FceRII expression on В cells are thus two closely related events. Supernatant fluid from FceRII-positive lymphoblastoid cell lines enhances IgE production by В cells from atopic individuals, suggesting soluble FceRII to enhance IgE production. Moreover, sFceRII increases in the serum of patients with collagen-vascular diseases such as systemic lupus erythematosus or rheumatoid arthritis and is correlated with disease activity. FceRII is both an autocrine and a paracrine В cell stimulatory factor and sFceRII may thus possibly be a parameter of В-cell activation.
In this study, measurement was made of serum levels of sIL-2R, IL-4, and sFceRII in adult asthmatics to confirm T-cell and В-cell activation in the pathogenesis of asthma and elucidate the mode of involvement of IL-4 and sFceRII in the regulation of IgE synthesis.