title: Natural killer cells accumulate in lung-draining lymph nodes and regulate airway eosinophilia in a murine model of asthma.
abstract: Increasing evidence suggests a key role for the innate immune system in asthma development. Although the role of Natural Killer (NK) cells in allergic asthma is poorly known, modifications of the blood NK cell populations have been found in asthmatic and/or allergic patients. Their repartition and activation status in the inflammatory (lungs) and the regulatory (draining lymph nodes) sites of the allergic reaction is unknown. The aim of our study was to monitor NK cell migration pattern and activation status and to investigate the consequences of NK cell depletion during allergic airway reaction in a mouse model. Ovalbumin sensitization and challenges of BALB/cByJ mice had no effect on the total number of lung NK cells but significantly decreased the number of most mature NK cells and increased the level of the activation marker CD86. In the lung-draining mediastinal lymph nodes, ovalbumin sensitization and challenges led to increased number of NK cells, and more precisely, immature NK cells and increased expression of CD86. Ovalbumin-sensitized mice also exhibited increased percentage of proliferating NK cells in lung-draining mediastinal lymph nodes. Anti-ASGM1 antibody treatment depleted most NK cells and decreased bronchoalveolar lavage eosinophilia but did not modify airway responsiveness. Altogether, our study shows that pulmonary allergic sensitization induces modification in the NK cell compartment at the inflammatory and regulatory sites and suggests that NK cells may participate in the regulation of the asthmatic response and, more particularly, to the allergic airway eosinophilia.
authors.affiliation: INSERM, Institut National de la Santé et de la Recherche Médicale U774, Lille, France.
authors.forename: C
authors.initials: C
authors.lastname: Ple
authors.forename: M
authors.initials: M
authors.lastname: Barrier
authors.forename: L
authors.initials: L
authors.lastname: Amniai
authors.forename: P
authors.initials: P
authors.lastname: Marquillies
authors.forename: J
authors.initials: J
authors.lastname: Bertout
authors.forename: A
authors.initials: A
authors.lastname: Tsicopoulos
authors.forename: T
authors.initials: T
authors.lastname: Walzer
authors.forename: P
authors.initials: P
authors.lastname: Lassalle
authors.forename: C
authors.initials: C
authors.lastname: Duez
mesh_terms: D000818:Animals; D000906:Antibodies / Q000097:blood / Q000276:immunology; D015703:Antigens, CD / Q000276:immunology; D001249:Asthma / Q000276:immunology* / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D049109:Cell Proliferation; D004802:Eosinophilia / Q000276:immunology*; D005260:Female; D007113:Immunity, Innate / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology* / Q000473:pathology; D008168:Lung / Q000276:immunology* / Q000473:pathology; D008198:Lymph Nodes / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology
chemical_list: D000906:Antibodies; D015703:Antigens, CD; D010047:Ovalbumin