1. Cutting Edge: Role of NK Cells and Surfactant Protein D in Dendritic Cell Lymph Node Homing: Effects of Ozone Exposure
- Author
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Ge, Moyar Qing, Kokalari, Blerina, Flayer, Cameron H, Killingbeck, Sarah S, Redai, Imre G, MacFarlane, Alexander W, Hwang, Jin W, Kolupoti, Anisha, Kemeny, Michael D, Campbell, Kerry S, and Haczku, Angela
- Subjects
Biomedical and Clinical Sciences ,Immunology ,Lung ,2.1 Biological and endogenous factors ,Aetiology ,Inflammatory and immune system ,Animals ,Chemotaxis ,Leukocyte ,Dendritic Cells ,Flow Cytometry ,Interferon-gamma ,Killer Cells ,Natural ,Lymph Nodes ,Male ,Mice ,Mice ,Inbred C57BL ,Ozone ,Pneumonia ,Pulmonary Surfactant-Associated Protein D ,Real-Time Polymerase Chain Reaction ,Biochemistry and cell biology - Abstract
The roles of NK cells, surfactant protein D (SP-D), and IFN-γ, as well as the effect of ozone (O3) inhalation, were studied on recirculation of pulmonary dendritic cells (DC) to the mediastinal lymph nodes. O3 exposure and lack of SP-D reduced NK cell IFN-γ and lung tissue CCL21 mRNA expression and impaired DC homing to the mediastinal lymph nodes. Notably, addition of recombinant SP-D to naive mononuclear cells stimulated IFN-γ release in vitro. Because NKp46, a glycosylated membrane receptor, was necessary for dose-dependent SP-D binding to NK cells in vitro and DC migration in vivo, we speculate that SP-D may constitutively stimulate IFN-γ production by NK cells, possibly via NKp46. This mechanism could then initiate the IFN-γ/IL-12 feedback circuit, a key amplifier of DC lymph node homing. Inhibition of this process during an acute inflammatory response causes DC retention in the peripheral lung tissue and contributes to injury.
- Published
- 2016