Rationale for targeting interleukin-17 in the lungs.
An increasing body of evidence suggests that an exaggerated accumulation of activated neutrophils in the airways can cause decline of the clinical state in several lung diseases, including acute, severe asthma. In spite of this, an effective pharmacotherapy against this type of exaggerated neutrophil activity has yet to be developed. This review presents the scientific rationale for targeting the T-cell cytokine interleukin (IL)-17 in inflammatory lung diseases, to normalize neutrophil activity. Evidence leads to the conclusion that the production and release of IL-17 orchestrates neutrophil activity in the lungs. Hypothetically, local blockade of IL-17 may prove effective to normalize exaggerated neutrophil activity in lung diseases.
Lindén
Anders
A
Lung Pharmacology Group, Department of Allergology and Respiratory Medicine, Institute of Internal Medicine, Göteborg University, Guldhedsgatan 10A, SE-41346 Gothenburg, Sweden. anders.linden@lungail.gu.se
D000818:Animals; D006801:Humans; D020381:Interleukin-17 / Q000037:antagonists & inhibitors / Q000276:immunology*; D008168:Lung / Q000276:immunology* / Q000378:metabolism; D008171:Lung Diseases / Q000276:immunology* / Q000378:metabolism; D018375:Neutrophil Activation / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism
D020381:Interleukin-17