Toll-like receptors are key players in neurodegeneration

Int Immunopharmacol. 2011 Oct;11(10):1415-21. doi: 10.1016/j.intimp.2011.05.006. Epub 2011 May 25.

Abstract

The activation of innate immune response is initiated by engagement of pattern-recognition receptors (PPRs), such as Toll-like receptors (TLRs). These receptors are expressed in peripheral leukocytes and in many cell types in the central nervous system (CNS). The expression of TLRs in CNS was mainly studied in astrocytes and microglial cells. However, new evidence indicates that these receptors may play an important role in neuronal homeostasis. The expression of TLRs in the CNS is variable and can be modulated by multiple factors, including pro-inflammatory molecules, which are elevated in neurodegenerative diseases and can increase the expression of TLRs in CNS cells. Moreover, activation of TLRs induces the release of pro-inflammatory cytokines. Therefore, TLRs have been shown to play a role in several aspects of neurodegenerative diseases. Here we will discuss results reported in the recent literature concerning the participation of TLRs in neurodegenerative diseases.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Astrocytes / immunology
  • Cell Survival / immunology
  • Cellular Microenvironment / immunology
  • Central Nervous System / immunology
  • Central Nervous System / metabolism*
  • Central Nervous System / pathology
  • Cytokines / immunology
  • Cytokines / metabolism*
  • Gene Expression Regulation / immunology
  • Humans
  • Inflammation
  • Inflammation Mediators / immunology
  • Inflammation Mediators / metabolism*
  • Microglia / immunology
  • Molecular Targeted Therapy
  • Neurodegenerative Diseases / drug therapy
  • Neurodegenerative Diseases / immunology*
  • Neurodegenerative Diseases / physiopathology
  • Neurons / physiology
  • Toll-Like Receptors / agonists
  • Toll-Like Receptors / antagonists & inhibitors
  • Toll-Like Receptors / immunology*

Substances

  • Cytokines
  • Inflammation Mediators
  • Toll-Like Receptors