Background Dendritic ceils （DCs） are the most important professional antigen presenting cells that play a key role in initiating adaptive immune responses. The depletion and dysfunction of DCs contribute to the deve...Background Dendritic ceils （DCs） are the most important professional antigen presenting cells that play a key role in initiating adaptive immune responses. The depletion and dysfunction of DCs contribute to the development of immunodeficiency or immunoparalysis in some lung diseases. In the present study, we investigated the effects of Fms-like tyrosine kinase-3 ligand （FIt3L） administration in vivo on lung DCs expansion to provide an experimental basis of FIt3L used as a potential therapeutic agent for the related lung disorders. Methods Balb/c mice were randomly divided into FIt3L group （n=10） and control group （n=10）. Each mouse in the FIt3L group received subcutaneous administration of FIt3L at a dose of 10 pg once daily for nine consecutive days. Lung histology was observed, and CD11c and CD205 were immunologically labeled in lung tissue sections. Low-density lung cells were separated by density gradient centrifugation, and then subsets and MHC-II/I-Ad expression of DCs were analyzed by flow cytometry. Results In the FIt3L group the number and density of DC-like cells were markedly increased compared with the control group, mainly distributed in the alveolar septa. Immunological labeling in situ found that there were significantly higher numbers of CD11c＋ and CD205＋ DCs in lung mesenchymal tissue （P 〈0.05）, where they formed a denser reticular formation. Flow cytometry analysis demonstrated that the proportions of myeloid CD11c＋CD11b＋ DCs and plasmacytoid CD11c＋CD45R/B220＋ DCs in the low-density lung cells in the FIt3L group were significantly higher compared with the control group; showing 3.17- and 3.3-fold increase respectively （P 〈0.05）. The proportion of CD11c＋ DCs expressing MHC-II/I-Ad＋ was significantly increased, with a 2.7-fold increase as compared with the control group （P 〈0.05）. Conclusions FIt3L administration in vivo induces lung DCs expansion, favoring myeloid and plasmacytoid DC subsets, which are phenotypically more mature. FIt3L may be useful in the therapy to augment immune function of the lung.展开更多
基金This research was supported by the grant from the National Natural Science Foundation of China （No. 81000848）.
文摘Background Dendritic ceils （DCs） are the most important professional antigen presenting cells that play a key role in initiating adaptive immune responses. The depletion and dysfunction of DCs contribute to the development of immunodeficiency or immunoparalysis in some lung diseases. In the present study, we investigated the effects of Fms-like tyrosine kinase-3 ligand （FIt3L） administration in vivo on lung DCs expansion to provide an experimental basis of FIt3L used as a potential therapeutic agent for the related lung disorders. Methods Balb/c mice were randomly divided into FIt3L group （n=10） and control group （n=10）. Each mouse in the FIt3L group received subcutaneous administration of FIt3L at a dose of 10 pg once daily for nine consecutive days. Lung histology was observed, and CD11c and CD205 were immunologically labeled in lung tissue sections. Low-density lung cells were separated by density gradient centrifugation, and then subsets and MHC-II/I-Ad expression of DCs were analyzed by flow cytometry. Results In the FIt3L group the number and density of DC-like cells were markedly increased compared with the control group, mainly distributed in the alveolar septa. Immunological labeling in situ found that there were significantly higher numbers of CD11c＋ and CD205＋ DCs in lung mesenchymal tissue （P 〈0.05）, where they formed a denser reticular formation. Flow cytometry analysis demonstrated that the proportions of myeloid CD11c＋CD11b＋ DCs and plasmacytoid CD11c＋CD45R/B220＋ DCs in the low-density lung cells in the FIt3L group were significantly higher compared with the control group; showing 3.17- and 3.3-fold increase respectively （P 〈0.05）. The proportion of CD11c＋ DCs expressing MHC-II/I-Ad＋ was significantly increased, with a 2.7-fold increase as compared with the control group （P 〈0.05）. Conclusions FIt3L administration in vivo induces lung DCs expansion, favoring myeloid and plasmacytoid DC subsets, which are phenotypically more mature. FIt3L may be useful in the therapy to augment immune function of the lung.
