Neutrophils, interleukin-17A and lung disease.
It 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.
Lindén
A
A
Cooperative Research Centre for Chronic Inflammatory Diseases, Dept of Pharmacology, The University of Melbourne, Medical Building, Level 8, W810, Grattan Street/Royal Parade, Parkville, VIC 3010, Australia. a.linden@unimelb.edu.au
Laan
M
M
Anderson
G P
GP
D015415:Biomarkers / Q000097:blood; D016207:Cytokines / Q000032:analysis / Q000378:metabolism; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D020381:Interleukin-17 / Q000276:immunology* / Q000378:metabolism; D008171:Lung Diseases / Q000276:immunology* / Q000503:physiopathology*; D008213:Lymphocyte Activation; D008297:Male; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism; D011379:Prognosis; D012307:Risk Factors; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
D015415:Biomarkers; D016207:Cytokines; D020381:Interleukin-17