Zbtb46 expression distinguishes classical dendritic cells and their committed progenitors from other immune lineages

By Ansuman T. Satpathy, Wumesh Kc, J. Albring, B. Edelson, Nicole M. Kretzer, Deepta Bhattacharya, T. Murphy, K. Murphy. Journal of Experimental Medicine, 2012

637 citations recorded by the source corpus.

The zinc finger transcription factor Zbtb46 specifically marks cDCs and their committed precursors and, when overexpressed in BM progenitors, promotes cDC development at the expense of granulocytes.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/0db25751f909c6ea01ac5f272f26c3fe0405fe63

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Florent Ginhoux
2. Steffen Jung
3. A. Mildner
4. Miriam Merad
5. C. Varol
6. G. Randolph
7. Y. Belkaid
8. K. Honda

Citations in the corpus

• The dendritic cell lineage: ontogeny and function of dendritic cells and their subsets in the steady state and the inflamed setting. (2013, background): “The zinc finger transcription factor zbtb46 is expressed on endothelial cells and erythroid progenitors, but its expression within the immune system is restricted to the cDC lineage (28, 29).”
• Ly6C hi monocytes in the inflamed colon give rise to proinflammatory effector cells and migratory antigen-presenting cells. (2012, methodology): “As revealed by the gene expression profiling and flow cytometer-based single-cell analysis of the inflamed colon of zbtb46/WT mice, the Ly6C cell population also displays prominent—though not homogeneous—expression of the transcription factor Zbtb46, proposed to be a cDC hallmark (Meredith et al., 2”
• Development and function of dendritic cell subsets. (2014, positive): “Pre-DCs of zbtb46-GFP reporter animals can indeed be subdivided according to expression of the lectin Siglec-H and zbtb46 (Satpathy et al., 2012).”
• Self-renewing resident cardiac macrophages limit adverse remodeling following myocardial infarction (2018, positive): “…presenting cell (APC) cluster (cluster 6) that expressed some macrophage and DC genes (Adgre1, C1qc, C1qa, MHC-II genes, Itgax) but not lineage defining genes (Fcgr1, Maf, Mertk, Dpp4, Flt3, Zbtb46) 22, 23 ; nor did this cluster have high expression of pDC genes (Siglech, Bst2, Ly6c2, Irf8) (Fig.”
• IRF4 Transcription Factor-Dependent CD11b+ Dendritic Cells in Human and Mouse Control Mucosal IL-17 Cytokine Responses (2013, methodology): “Supporting these data, the DC lineagerestricted TF Zbtb46 is highly expressed in the CD24 fraction of lung MHCIICD11cCD11b and gut LP MHCIICD11c CD11bCD103 populations (Satpathy et al., 2012).”
• Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation (2014, background): “Both DC subsets expressed high amounts of the classic dendritic cell (DC) transcription factor Zbtb46 (Figure 1D) (Satpathy et al., 2012).”
• Human inflammatory dendritic cells induce Th17 cell differentiation. (2013, methodology): “Finally, mouse Mo-DCs express the DC lineage-specific transcription factor Zbtb46 (Satpathy et al., 2012), and CSF1R/ CD115 has recently been shown to be important for mouse infDC development in vivo (Greter et al.”
• Minimal differentiation of classical monocytes as they survey steady state tissues and transport antigen to lymph nodes (2013, background): “Recent data also suggest they do not give rise to DCs in the lung (Satpathy et al., 2012).”
• Two distinct interstitial macrophage populations coexist across tissues in specific subtissular niches (2019, background): “As expected, bothLyve1hiMHCIIlo andLyve1loMHCIIhi macrophages, like lung monocytes and AMs, did not express ZBTB46 comparedwith classical DCs (fig.”
• The tumor microenvironment at a glance (2012, background): “Two recent studies designate ZBTB46 as a new transcription factor that is specifically expressed in all classical human and murine DCs (Meredith et al., 2012; Satpathy et al., 2012).”