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Copyright ©ERS Journals Ltd 2005
Neutrophils, interleukin-17A and lung disease
Cooperative Research Centre for Chronic Inflammatory Diseases, Depts of Medicine and Pharmacology, University of Melbourne, Melbourne, Australia
CORRESPONDENCE: A. Lindén, 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. Fax: 61 383440246. E-mail: a.linden@unimelb.edu.au
Keywords: Cytotoxic T-lymphocyte-associated serine esterase-8, innate immunity, interleukin-17, T-lymphocytes
Received: March 16, 2004
Accepted August 5, 2004
ABSTRACT
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.
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