Journal
IMMUNITY
Volume 45, Issue 5, Pages 975-987Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2016.10.011
Keywords
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Categories
Funding
- AHA Fellowships [16POST27630002, 12DG12070005]
- Ruth L. Kirschstein National Research Service Award (NRSA) Institutional Predoctoral Training Grant, from National Institute of General Medical Sciences [T32 GM008666]
- [R01HL134236]
- [R01HL118765]
- [R01CA202987]
- [R01HL112039]
- [R01DK091183]
- [R01CA17390]
- [R01HL088093]
- [R00HL123485]
- [R01GM086912]
- [R01HL086548]
- [R01075427]
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Mononuclear phagocytes are a heterogeneous family that occupy all tissues and assume numerous roles to support tissue function and systemic homeostasis. Our ability to dissect the roles of individual subsets is limited by a lack of technologies that ablate gene function within specificmononuclear phagocyte sub-populations. Using Nr4a1-dependent Ly6C(low) monocytes, we present a proof-of-principle approach that addresses these limitations. Combining ChIP-seq and molecular approaches we identified a single, conserved, sub-domain within the Nr4a1 enhancer that was essential for Ly6C(low) monocyte development. Mice lacking this enhancer lacked Ly6C(low) monocytes but retained Nr4a1 gene expression in macrophages during steady state and in response to LPS. Because Nr4a1 regulates inflammatory gene expression and differentiation of Ly6C(low) monocytes, decoupling these processes allows Ly6C(low) monocytes to be studied independently.
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