The IL-1β phenomena in neuroinflammatory diseases

J Neural Transm (Vienna). 2018 May;125(5):781-795. doi: 10.1007/s00702-017-1732-9. Epub 2017 May 22.

Abstract

It is becoming increasingly clear that neuroinflammation has a causal role in the pathogenesis of central nervous system (CNS)-related diseases, and therefore therapeutic strategies targeting the regulation or availability of inflammatory mediators can be used to prevent or mitigate pathology. Interestingly, the proinflammatory cytokine, interleukin-1 beta (IL-1β), has been implicated in perpetuating immune responses and contributing to disease severity in a variety of CNS diseases ranging from multiple sclerosis, neurodegenerative diseases, traumatic brain injury, and diabetic retinopathy. Moreover, pharmacological blockade of IL-1 signaling has shown to be beneficial in some autoimmune and autoinflammatory diseases, making IL-1β a promising therapeutic target in neuroinflammatory conditions. This review highlights recent advances of our understanding on the multifaceted roles of IL-1β in neuroinflammatory diseases.

Keywords: Alzheimer’s disease; Diabetic retinopathy; IL-1β; Microglia; Multiple sclerosis; Neuroinflammation.

Publication types

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

MeSH terms

  • Animals
  • Central Nervous System Diseases / immunology*
  • Central Nervous System Diseases / pathology*
  • Humans
  • Inflammation / immunology*
  • Inflammation / pathology*
  • Interleukin-1beta / immunology*

Substances

  • Interleukin-1beta