Brains, Blood, and Guts: MeCP2 Regulates Microglia, Monocytes, and Peripheral Macrophages

Dorothy P Schafer1, Beth Stevens2

  • 1Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.

Immunity
|April 23, 2015
PubMed

Insights

Mutations in methyl-CpG-binding protein 2 (MECP2) cause Rett Syndrome. Studies show MeCP2 deficiency alters macrophage function, impacting immune and stress responses in mice.

Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Mutations in methyl-CpG-binding protein 2 (MECP2) are the primary cause of Rett Syndrome, a severe neurodevelopmental disorder.
  • Rett Syndrome is characterized by significant neurological and somatic impairments, affecting multiple bodily systems.

Purpose of the Study:

  • To investigate the role of MeCP2 in the function of macrophages.
  • To determine how MeCP2 deficiency impacts immune cell responses in the context of Rett Syndrome.

Main Methods:

  • Utilizing a mouse model with MeCP2 deficiency.
  • Analyzing macrophage populations and their responses to various stimuli, including glucocorticoids, hypoxia, and inflammatory signals.

Main Results:

  • Macrophage populations were found to be abnormal in number in MeCP2-deficient mice.
  • These macrophages exhibited altered responses to glucocorticoid, hypoxia, and inflammatory stimuli.

Conclusions:

  • MeCP2 plays a critical role in regulating macrophage number and function.
  • Dysfunctional macrophages due to MeCP2 deficiency may contribute to the pathophysiology of Rett Syndrome.