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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
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CITED2 limits pathogenic inflammatory gene programs in myeloid cells.

Hang Pong Ng1, Gun-Dong Kim1, E Ricky Chan2

  • 1Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|July 23, 2020
PubMed
Summary
This summary is machine-generated.

CBP/p300-interacting transactivator with glutamic acid/aspartic acid-rich carboxyl-terminal domain 2 (CITED2) acts as a key regulator, preventing excessive inflammation by controlling macrophage pro-inflammatory responses. CITED2 restrains NFκB activation, maintaining immune balance.

Keywords:
CITED2inflammationinnate immunitymacrophage

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Macrophages are crucial innate immune cells responding to inflammation.
  • Uncontrolled macrophage activation can lead to detrimental inflammatory conditions.
  • Endogenous mechanisms are essential for regulating macrophage responses.

Purpose of the Study:

  • To identify intrinsic regulators of macrophage inflammation.
  • To investigate the role of CITED2 in controlling pro-inflammatory responses.
  • To elucidate the molecular mechanisms by which CITED2 modulates macrophage activation.

Main Methods:

  • In vivo studies of myeloid-specific CITED2-deficient mice.
  • Integrated transcriptomics and gene set enrichment analysis (GSEA).
  • Gain- and loss-of-function studies with CITED2 overexpression/deficiency.
  • Analysis of NFκB transcriptional activity and p65 recruitment.
  • NFκB signaling blockade experiments.

Main Results:

  • Myeloid-CITED2 deficiency increased macrophage and neutrophil recruitment.
  • CITED2 deficiency broadly enhanced NFκB targets and inflammatory gene expression.
  • CITED2 regulates LPS-induced NFκB activity and p65 promoter recruitment.
  • NFκB blockade reversed the pro-inflammatory gene expression in CITED2-deficient macrophages.

Conclusions:

  • CITED2 is a critical intrinsic negative regulator of inflammation in macrophages.
  • CITED2 restrains NFκB activation, thereby curtailing pro-inflammatory gene programs.
  • CITED2 plays a vital role in maintaining immune homeostasis by controlling macrophage activation.