• Mihnea T Zdrenghea, Patrick Mallia, and Sebastian L Johnston.
• Oncology Institute Prof. Dr. Ion Chiricuta, Department of Hematology and University of Medicine and Pharmacy Cluj-Napoca, Romania. mzdrenghea@umfcluj.ro
• Eur. J. Clin. Invest. 2012 Sep 1; 42 (9): 1010-5.

BackgroundChronic obstructive pulmonary disease (COPD) is characterized by high levels of antiviral type 1 cytokine interferon-γ and activated CD8(+) T cells. COPD exacerbations are the major cause of morbidity and mortality, have a prolonged and intense effect on quality of life and may result in accelerated loss of lung function. Respiratory virus infections, frequently within a state of colonization by bacteria, are the major cause of COPD exacerbations, and there is also evidence of virus latency in 'stable' disease, suggesting that latent infection might be a cause of chronic inflammation in COPD.DesignThis is an update of current literature concerning the role of interleukin-15 and major histocompatibility complex class I-related chain A and B molecules in type 1 immune responses, particularly to respiratory virus infections, which are the main cause of COPD exacerbations. We also present data from our own group suggesting a role for interleukin-15 in virus-induced COPD exacerbations.ResultsType 1 cytokine interleukin-15 is produced by resident airway cells (epithelial cells and macrophages) in response to virus infection and bacteria. Virus infections modulate major histocompatibility complex class I-related chain A and B molecules in respiratory epithelial cells.ConclusionsInterleukin-15 could play a major role in the airway inflammation in COPD directly, via its own receptors, by amplifying the type 1 immune responses and decreasing apoptosis or indirectly, via modulating molecules associated with cytotoxic activity of natural killer and CD8(+) T cells, such as major histocompatibility complex class I-related chain A and B.© 2012 The Authors. European Journal of Clinical Investigation © 2012 Stichting European Society for Clinical Investigation Journal Foundation.

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