Peripheral T cells derived from Alzheimer's disease patients overexpress CXCR2 contributing to its transendothelial migration, which is microglial TNF-alpha-dependent

Neurobiol Aging. 2010 Feb;31(2):175-88. doi: 10.1016/j.neurobiolaging.2008.03.024.

Abstract

The mechanism of circulating T cells entry into the brain in Alzheimer's diseases (AD) remains unclear. Here, we showed that peripheral T cells derived from AD patients overexpress CXCR2 to enhance its transendothelial migration. T cells migration through in vitro blood-brain barrier model was effectively blocked by anti-CXCR2 antibody or IL-8 (a CXCR2 ligand) RNAi in human brain microvascular endothelial cells (HBMECs). Amyloid beta (Abeta) injection in rat hippocampus upregulated CXCR2 expression accompanied with increased T cells occurrence in the brain, and this enhanced T cells entry was effectively blocked by CXCR2 antagonist. Furthermore, anti-TNF-alpha antibody blocked IL-8 production in HBMECs and T cells transendothelial migration caused by the culture supernatant of microglia treated with Abeta. Blockage of intracerebral TNF-alpha abolished the upregulation of CXCR2 in peripheral T cells and the increased T cells occurrence in the brain induced by Abeta injection in rat hippocampus. These data suggest that CXCR2 overexpression in peripheral T cells is intracerebral microglial TNF-alpha-dependent and TNF-alpha primes T cells transendothelial migration in Alzheimer's diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Autoantibodies / metabolism
  • Blood-Brain Barrier / drug effects
  • Blood-Brain Barrier / physiopathology*
  • Brain / blood supply
  • Brain / drug effects
  • Brain / physiopathology
  • Cell Movement / drug effects
  • Cell Movement / physiology*
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / physiopathology*
  • Female
  • Humans
  • Interleukin-8 / metabolism
  • Male
  • Microglia / metabolism
  • Microvessels / drug effects
  • Microvessels / physiopathology
  • Rats
  • Rats, Wistar
  • Receptors, Interleukin-8B / antagonists & inhibitors
  • Receptors, Interleukin-8B / immunology
  • Receptors, Interleukin-8B / metabolism*
  • T-Lymphocytes / physiology*
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Amyloid beta-Peptides
  • Autoantibodies
  • Interleukin-8
  • Receptors, Interleukin-8B
  • Tumor Necrosis Factor-alpha