| First Author | Ge MQ | Year | 2016 |
| Journal | J Immunol | Volume | 196 |
| Issue | 2 | Pages | 553-7 |
| PubMed ID | 26673133 | Mgi Jnum | J:254484 |
| Mgi Id | MGI:6101973 | Doi | 10.4049/jimmunol.1403042 |
| Citation | Ge MQ, et al. (2016) Cutting Edge: Role of NK Cells and Surfactant Protein D in Dendritic Cell Lymph Node Homing: Effects of Ozone Exposure. J Immunol 196(2):553-7 |
| abstractText | The roles of NK cells, surfactant protein D (SP-D), and IFN-gamma, 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-gamma 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-gamma 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-gamma production by NK cells, possibly via NKp46. This mechanism could then initiate the IFN-gamma/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. |
