MECHANISMS OF ALLERGY AND ADULT ASTHMA: Edited by J Andrew Grant and Gustavo J RodrigoNatural killer cells in asthmaGorska, Magdalena M.a,b Author Information aNational Jewish Health, Denver bUniversity of Colorado, Aurora, Colorado, USA Correspondence to Magdalena M. Gorska, National Jewish Health, Department of Medicine, Division of Allergy and Clinical Immunology, 1400 Jackson St, Denver, CO 80206, USA. Tel: +1 303 398 1656; fax: +1 303 298 1806; e-mail: [email protected] Current Opinion in Allergy and Clinical Immunology 17(1):p 50-54, February 2017. | DOI: 10.1097/ACI.0000000000000327 Buy Metrics Abstract Purpose of review This review article discusses current knowledge on natural killer (NK) cells in asthma. Recent findings It is now well accepted that NK cell activities go beyond cancer immune surveillance and antiviral defense. Recent reports indicate that NK cells are activated in response to allergens in vivo. NK cells promote allergic sensitization, type-2 immune response, development of eosinophilic inflammation, and airway hyperresponsiveness. NK cells are activated by respiratory syncytial virus and other respiratory viruses. When infection occurs in the setting of active allergic inflammation, NK cells augment its magnitude and contribute to asthma exacerbations. Proasthma activities of NK cells can be programmed during embryogenesis through maternal exposure to environmental pollutants. Prenatally programmed NK cells produce type-2 and type-3 cytokines and mediate asthma predisposition. NK cells can also act as asthma antagonists. NK cells contribute to the resolution of inflammation through suppression of antigen-specific CD4+ T cells and type-3 immunity. When viral infection occurs in naïve mice prior to allergic sensitization, NK cells antagonize type-2 immunity and prevent development of asthma. Summary NK cells are nonredundant participants of allergic inflammation. The environmental context determines whether NK cells act as protagonists or antagonists. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.