Spineless Behavior of CX3CR1+ Monocytes in Response to Infection

Immunity. 2017 Jul 18;47(1):12-14. doi: 10.1016/j.immuni.2017.06.022.

Abstract

Sickness in mammals can lead to cognition deficits, although the underlying mechanisms remain elusive. In a recent Nature Medicine article, Garré et al. (2017) report that sickness-induced cortical dendritic spine loss and impaired memory formation is mediated by CX3CR1+ monocyte-derived TNF-α.

Publication types

  • Comment

MeSH terms

  • Animals
  • CX3C Chemokine Receptor 1
  • Dendritic Spines / physiology*
  • Humans
  • Memory
  • Mental Disorders / etiology
  • Mental Disorders / immunology*
  • Mental Disorders / psychology
  • Mice
  • Monocytes / physiology*
  • Monocytes / virology
  • Motor Neurons / physiology*
  • Motor Neurons / virology
  • Nerve Net*
  • Neuronal Plasticity*
  • Poly I-C / immunology
  • Receptors, Chemokine / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Virus Diseases / complications
  • Virus Diseases / immunology*
  • Virus Diseases / psychology

Substances

  • CX3C Chemokine Receptor 1
  • Cx3cr1 protein, mouse
  • Receptors, Chemokine
  • Tumor Necrosis Factor-alpha
  • Poly I-C