Lung is a complex organ which is responsible for air conduction, gas exchange and host defense. It has been found several types of lung stem/ progenitor cells in different portions to maintain local tissue homeostasis. In the previous study, we had identified a new subset of lung stem/ progenitor cells from neonatal mice, SSEA-1+ pulmonary stem/ progenitor cells (SSEA-1+ PSCs). SSEA-1+ PSCs are self-renewal and exhibit the multi-potencies to differentiate into ciliate cells and alveolar cells in vitro. Interestingly, we also found that SSEA-1+ PSCs but not SSEA-1 negative populations are able to suppress allergic airway inflammation in the OVA-induced allergic asthma mouse model. And SSEA-1+ PSCs inhibit TSLP and eotaxin production by lung epithelial cells during stimulation in a cell contact-independent mechanisms. To get more insights and the application of SSEA-1+ PSCs, we also now focused on the studies in mechanisms of SEA-1+ PSCs self-renewal and immune regulation. In this study, we found that mouse embryonic fibroblasts (MEFs) could be used as feeder cells for SSEA-1+ PSCs. In comparison to SSEA-1+ PSCs alone, cell co-cultured with MEFs showed higher ability in maintenance of Nanog expreesion. Nanog is a stem cell-related factor expressed in fresh isolated SSEA-1+ PSCs but not in differentiated cells. After cell co-culture, SSEA-1+ PSCs still exhibit the potency to be differentiated into the type I alveolar cells with no detectable Nanog expression. It suggested that the stem-ness of SSEA-1+ PSCs can be maintained by MEFs in vitro. Based on microarray analysis, there are some transcriptional factors that are higher expressed in SSEA-1+ PSCs than those of other lung epithelial cells. These factors are involved in stem cell self-renewal and lung morphogenesis, including Bmi1, Foxa2, Nkx2.1 and Sox15. We will then study whether these factors are important in SSEA-1+ PSCs self-renewal and immune regulation.