| First Author | Dicken J | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 10 | Pages | e77490 |
| PubMed ID | 24204843 | Mgi Jnum | J:290080 |
| Mgi Id | MGI:6236616 | Doi | 10.1371/journal.pone.0077490 |
| Citation | Dicken J, et al. (2013) Transcriptional reprogramming of CD11b+Esam(hi) dendritic cell identity and function by loss of Runx3. PLoS One 8(10):e77490 |
| abstractText | Classical dendritic cells (cDC) are specialized antigen-presenting cells mediating immunity and tolerance. cDC cell-lineage decisions are largely controlled by transcriptional factor regulatory cascades. Using an in vivo cell-specific targeting of Runx3 at various stages of DC lineage development we show that Runx3 is required for cell-identity, homeostasis and function of splenic Esam(hi) DC. Ablation of Runx3 in DC progenitors led to a substantial decrease in splenic CD4(+)/CD11b(+) DC. Combined chromatin immunoprecipitation sequencing and gene expression analysis of purified DC-subsets revealed that Runx3 is a key gene expression regulator that facilitates specification and homeostasis of CD11b(+)Esam(hi) DC. Mechanistically, loss of Runx3 alters Esam(hi) DC gene expression to a signature characteristic of WT Esam(low) DC. This transcriptional reprogramming caused a cellular change that diminished phagocytosis and hampered Runx3(-/-) Esam(hi) DC capacity to prime CD4(+) T cells, attesting to the significant role of Runx3 in specifying Esam(hi) DC identity and function. |
