Interleukin-5 (IL5) is a T cell-derived cytokine involved in the pathogenesis of atopic diseases. It specifically controls the production, the activation and the localization of Eosinophils. The Eosinophils are the major cause of tissue damage resulting in the symptoms of asthma and related allergic disorders. T cells purified from bronchoalveolar lavage and peripheral blood of asthmatics secrete elevated amount of IL5. Therefore IL5 emerges to be an attractive target for the generation of new anti-allergic drugs. Agents which inhibit either the production or the activity of IL5 could be expected to ameliorate the pathological effects of the allergic response. A better understanding of the biology of IL5 and the regulation of its expression is, however, a prerequisite for the development of new therapeutic agents. This review covers the major biological, molecular and structural aspects of IL5 research since the identification of this cytokine ten years ago.
Earlier research indicates that within the human population there are considerable differences in the response to the carcinogenic activity of environmental carcinogens. Genetic polymorphism associated with several variants of the gene products participating in the biotransformation of various xenobiotics (including carcinogens) found in human populations constitutes a major cause of those differences. Enzymes coded by different variants of the same gene can differ in their catalytic activities. Up to the present time, most information on the effect of genetic polymorphism on the individual's ability to activate or deactivate environmental carcinogenic xenobiotics, and the associated risk of cancer, has been collected from studies of cytochromes P-450 belonging to gene families CYP1, CYP2 and CYP3, and of glutathione S-transferases and N-acetyltransferases. As carcinogen metabolism comprises a chain of chemical reactions involving numerous enzymes and enzyme-coding genes, research performed hitherto is able to offer only a very limited explanation of the associations between genetic polymorphism and the individual's susceptibility to cancer.
Detecting changes that precede the overt symptoms of cancer and identifying measurable indices of such changes in persons exposed to occupational and environmental carcinogens constitutes one of the primary objectives of molecular epidemiology research. Biomarkers represent a valuable research tool that makes it possible to attain that objective. Suitably selected biomarker sets may provide information on the extent of exposure to carcinogenic agents (internal dose, biologically effective dose), detect early changes caused by those agents in the exposed organism, and identify individuals with a particularly high risk of cancer development. The tremendous progress in research on the mechanisms of cancer initiation and promotion has enabled the assessment of cancer risk in healthy individuals by examining specific results from determinations of suitably selected biomarkers. The finding that gene defects (gene mutations and changes of their expression) constitute the background of carcinogenesis has resulted in molecular biology becoming focused on detecting defective genes or proteins synthesized under control of the defective genes.
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