It has been convincingly demonstrated that in patients with chronic obstructive pulmonary disease (COPD), chronic inflammation is present not only in the lung but extends outside the organ, in - volving regional lymph nodes and systemic circulation. Inflammatory cell profile in patients with COPD had higher numbers of B and CD4+, and especially CD8+ T lymphocytes, neutrophils, macrophages and it showes that innate immunity also plays a key role in pathogenesis of this disease. Inflammatory cells, which participate actively in the inflammatory response that characterizes COPD, produce a number of cytokines such as IL-6, TNF-a, IL-ip, TGF-pi, GM-CSF etc. Antigens causing COPD are debated. Chronic obstructive pulmonary disease is caused by the interaction of genetic susceptibility with environmental factors (especially smoking); however, genetic features of COPD disease still remain unknown. A large number of candidate genes for chronic obstructive pulmonary disease have already been identified in many experimental and clinical studies; however, polygenic etiology of chronic obstructive pulmonary disease is the main reason for conflicting molecular and genetic findings.
Since the pathology of COPD is that of a chronic inflammatory process with tissue damage and repair processes, it is not surprising that many cytokines play a role in this condition. One of the main focuses of research on cytokines is the determination of ways in witch the effects of these cytokines or their production may be regulated.
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