الفهرس 
review of literatureOnly 14 pages are availabe for public view
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Abstract
Apoptosis is a distinct form of cell death controlled by an internally encoded suicide program. It is a distinct event that triggers characteristic morphological and biological changes in the cellular life cycle. It is common during embryogenesis, normal tissue and organ involution, and cytotoxic immunological reactions and occurs naturally at the end of the life span of differentiated cells. Apoptosis can also be induced in cells by the application of a number of different agents, including physiological activators, heat shock, bacterial toxins, oncogenes, chemotherapeutic drugs, a variety of toxic chemicals, and ultraviolet and gamma radiation. Allergy is characterized by the accumulation of activated eosinophils at the site of inflammation. Inhibition of eosinophil apoptosis has been proposed as a key mechanism for the development of tissue eosinophilia in allergic disorders. The cytokines such as IL-3, IL-5, and GM-CSF are crucial mediators for eosinophil accumulation and survival in the allergic inflammatory sites, and depletion of these cytokines promotes spontaneous eosinophil apoptosis in vivo and in vitro. For the past decade, pharmacologic management of atopic diseases including bronchial asthma, allergic rhinitis, and atopic dermatitis has substantially progressed. This success is thought to be derived from advances in understanding pathophysiology of these diseases and development of anti-inflammatory drugs and improvement of their use, based on newly discovered mechanisms of the diseases. In the treatment of patients with allergic diseases, glucocorticoids have long been extensively used with remarkable success. Corticosteroids elicit apoptosis in inflammatory cells such as eosinophils and T lymphocytes, and suppress the production and release of both inflammatory eicosanoids and cytokines. This in part explains the potent antiinflammatory effects of corticosteroids in asthma patients.