As shown in Fig. 5, Flt3L gene expression was significantly increased in MPPs from Fli-1∆CTA/∆CTA B6 selleck kinase inhibitor mice compared with that cultured from wild-type B6 mice. The expressions of STAT3, Csf1 and Flt3

were higher in MPPS from Fli-1∆CTA/∆CTA B6 mice compared with that cultured from wild-type B6 mice, though the difference was not statistically significant (Fig. 5). To assess whether Fli-1 directly or indirectly regulates the expression of Flt3L, we analysed the promoter region of the Flt3L gene. There are 15 putative Fli-1 binding sites in the promoter region of the mouse Flt3L gene. We designed 15 pairs of primers to cover these sites, and a ChIP assay was performed to examine if Fli-1 binds to the promoter of Flt3L. The primers used are listed in Table 1. We examined the expression of Fli-1 and Flt3L in MS1 endothelial cell lines by RT-PCR and found that both Fli-1 and Flt3L are expressed in the cell line (data not shown). After immunoprecipitation by a Fli-1-specific antibody with cross-linked protein/DNA complexes from MS1 cell lines, two Fli-1 sites were significantly enriched with specific Fli-1 antibodies as detected by PCR amplification and compared with normal rabbit IgG controls (Fig. 6). These results clearly indicate Fli-1 can directly bind to the promoter of the Flt3L gene and probably regulate the expression of Flt3L. Fli-1 transcription factor regulates the differentiation

and development of haematopoietic lineages, especially megakaryocytic and erythrocytic lineages.[28-30] We previously demonstrated that Fli-1 modulates B-cell development and is implicated in autoimmune this website disease.[22, 26, 27, 31] We report here that Fli-1 also plays an important role in mononuclear phagocyte

development. We found that Fli-1∆CTA/∆CTA mice had significantly increased populations of HSCs and CDPs in BM compared with wild-type littermates (Fig. 1). Therefore, Fli-1 is likely to play an important role in regulating HSC and CDP development. Expression of Fli-1 clearly affects the HSC population and lack of the CTA domain in Fli-1 resulted in the increase of the HSC population. Previous studies have demonstrated that expression of Fli-1 affects development and differentiation Protein kinase N1 of megakaryocytes, erythrocytes, neutrophils and monocytes in Fli-1-deficient or Fli-1 heterozygous mice.[28, 29] Complete Fli-1 deficiency in HSCs resulted in a decrease in neutrophilic granulocyte and monocyte populations in mice.[29] In this report, we used Fli-1ΔCTA/ΔCTA mice with expression of a truncated Fli-1 protein, lacking the C-terminal transcriptional activation domain.[24] Cell proportion and absolute cell number of pDCs, cDCs, pre-cDCs and macrophages in the spleen from Fli-1∆CTA/∆CTA mice were significantly increased when compared with wild-type littermates (Fig. 2). The splenic cDC population can be subdivided into three groups according to their surface markers.