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lüll Neutrophils, interleukin-17A and lung disease Linden A; Laan M; Anderson GPEur Respir J 2005[Jan]; 25 (1): 159-72It is now established that an excessive and sustained mobilisation of neutrophils is a hallmark of several chronic inflammatory lung disorders, including severe obstructive lung disease. This article reviews evidence that the cytokine interleukin (IL)-17A is a major orchestrator of sustained neutrophilic mobilisation. Current evidence suggests that IL-17A is produced by T-lymphocytes, and that it exerts an orchestrating effect on the accumulation and associated activity of neutrophils in the bronchoalveolar space indirectly, through an induced release of specific cytokines and colony-stimulating factors in resident lung cells. Although the involvement of IL-17A in inflammatory lung disorders is supported by several recent studies, its causative role is still uncertain. However, the unique position of interleukin-17A at the interface between acquired and innate immunity puts this cytokine forward as an important signal for the reinforcement of host defence; it also implies that interleukin-17A may constitute a useful target for pharmacotherapeutic intervention.|Biomarkers/blood[MESH]|Cytokines/analysis/metabolism[MESH]|Female[MESH]|Humans[MESH]|Immunity, Innate/*physiology[MESH]|Interleukin-17/*immunology/metabolism[MESH]|Lung Diseases/*immunology/*physiopathology[MESH]|Lymphocyte Activation[MESH]|Male[MESH]|Neutrophils/*immunology/metabolism[MESH]|Prognosis[MESH]|Risk Factors[MESH]|Sensitivity and Specificity[MESH]|Severity of Illness Index[MESH]|T-Lymphocytes/*immunology/metabolism[MESH] |