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NTIS 바로가기Apoptosis : an international journal on programmed cell death, v.5 no.5, 2000년, pp.473 - 485
Vignola, Antonio M. (Istituto di Fisiopatologia Respiratoria, C.N.R., Via Trabucco, Palermo, Italy) , Chiappara, Giuseppina (Istituto di Fisiopatologia Respiratoria, C.N.R., Via Trabucco, Palermo, Italy) , Gagliardo, Rosalia (Istituto di Fisiopatologia Respiratoria, C.N.R., Via Trabucco, Palermo, Italy) , Gjomarkaj, Mark (Istituto di Fisiopatologia Respiratoria, C.N.R., Via Trabucco, Palermo, Italy) , Merendino, Anna (Clinica di Malatie Respiratorie, Università) , Siena, Liboria (di Palermo, Italy) , Bousquet, Jean (Istituto di Fisiopatologia Respiratoria, C.N.R., Via Trabucco, Palermo, Italy) , Bonsignore, G. (Clinique des Maladies Respiratoires and INSERM U 454, Hô)
Asthma is a disease characterized by a chronic inflammation of the airways and by structural alterations of bron-chial tissues, often referred to as airway remodelling. The development of chronic airway inflammation in asthma depends upon the continuous recruitment of inflammatory cells from the bloodstream towards the bronchial mucosa and by their subsequent activation. It is however increasingly accepted that mechanisms involved in the regulation of the survival and apoptosis of inflammatory cells may play a central role in the persistent inflammatory process characterizing this disease. Increased cellular recruitment and activation, enhanced cell survival and cell:cell interactions are therefore the key steps in the development of chronic airway inflammation in asthma, and represent the major causes for tissue damge, repair and remodelling.
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