期刊
JOURNAL OF IMMUNOLOGY
卷 196, 期 2, 页码 553-557出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1403042
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资金
- National Institutes of Health [R01AI072197]
- National Institutues of Health [R21AI083859]
- National University of Singapore President's Graduate Fellowship
The roles of NK cells, surfactant protein D (SP-D), and IFN-gamma, as well as the effect of ozone (O-3) inhalation, were studied on recirculation of pulmonary dendritic cells (DC) to the mediastinal lymph nodes. O-3 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.
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