Disruption of immune cell function by mutant huntingtin in Huntington's disease pathogenesis

Curr Opin Pharmacol. 2016 Feb:26:33-8. doi: 10.1016/j.coph.2015.09.008. Epub 2015 Oct 19.

Abstract

Innate immune dysfunction is increasingly recognised as a key characteristic of neurodegenerative disease. In the fatal inherited neurological disorder, Huntington's disease, altered innate immune cell function and increased inflammation are observed in the brain and the periphery of disease gene carriers many years before symptom onset, suggesting a potentially early and important role in disease pathogenesis. This is due, at least in part, to the intrinsic effects of the disease-causing protein, mutant huntingtin, expressed in innate immune cells themselves. Understanding whether such innate immune dysfunction in Huntington's disease can be targeted to slow the onset and/or the progression of the disease has significant therapeutic implications and is the subject of much current research.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Central Nervous System / immunology
  • Humans
  • Huntingtin Protein
  • Huntington Disease / genetics*
  • Huntington Disease / immunology*
  • Immunity, Innate
  • Inflammation / immunology
  • Microglia / immunology
  • Mutation
  • Myeloid Cells / immunology
  • Nerve Tissue Proteins / genetics*
  • Nerve Tissue Proteins / immunology*

Substances

  • HTT protein, human
  • Huntingtin Protein
  • Nerve Tissue Proteins