Abstract
Most chronic inflammatory diseases have been treated for several years now with steroids and anti-inflammatory drugs. While these treatment have certainly been effective the broad pharmacological effects of these treatments can lead to side effects. However, the advances made in the area of dissecting the pathogenesis of chronic diseases at the cellular and molecular level has, for the first time, provided the opportunity to target cell-specific molecules. Asthma, in particular, is a chronic inflammatory disease that has been studied in great detail. It is now well-accepted that the number of many types of inflammatory cells are increased in asthma and could be responsible for the tissue destruction and clinical sequelae. Eosinophils, for instance, by virtue of their large numbers in pulmonary inflammatory infiltrates and their destructive potential probably play a very significant role. Over the last ten to fifteen years, the understanding of T cell biology has increased dramatically and many inflammatory diseases such as asthma are being seen as having a significant pathogenic component at the level of T cell reactivity. Asthma is characterized by a polarized T helper cell response, and a number of studies both in animal models and human subjects indicate that the predominant T helper cell involved in allergic disease is the TH2 cell type. T helper subsets can be divided into two major subtypes, the TH1 subtype being primarily responsible for cell mediated immunity and the TH2 for the humoral response including IgE. TH1 cells can be identified based on the release of IL-2 and IFNγ and the TH2 subtype on the secretion of IL-4, IL-5 and IL-10.
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Cuss, F.M. (2000). Interleukin 5. In: Narula, S.K., Coffman, R. (eds) New Cytokines as Potential Drugs. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8456-3_1
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