Triggering receptor expressed on myeloid cells-2 is involved in prion-induced microglial activation but does not contribute to prion pathogenesis in mouse brains

Caihong Zhu, Uli S. Herrmann, Bei Li, Irina Abakumova, Rita Moos, Petra Schwarz, Elisabeth J. Rushing, Marco Colonna, Adriano Aguzzi

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Dysfunctional variants of the innate immune cell surface receptor TREM2 (triggering receptor expressed on myeloid cells-2) were identified as major genetic risk factors for Alzheimer's disease and other neurodegenerative conditions. Here we assessed a possible involvement of TREM2 in prion disease. We report that TREM2 expression by microglia is significantly up-regulated upon prion infection. However, depletion of TREM2 did not affect disease incubation time and survival after intracerebral prion infection. Interestingly, markers of microglial activation were attenuated in prion-infected TREM2-/- mice, suggesting an involvement of TREM2 in prion-induced microglial activation. Further phenotype profiling of microglia revealed that TREM2 deficiency did not change microglial phenotypes. We conclude that TREM2 is involved in prion-induced microglial activation but does not noticeably modulate the pathogenesis of experimental prion infections.

Original languageEnglish
Pages (from-to)1994-2003
Number of pages10
JournalNeurobiology of Aging
Volume36
Issue number5
DOIs
StatePublished - 2015

Keywords

  • Microglial activation
  • Neuroinflammation
  • Pathogenesis
  • Prion disease
  • TREM2

Fingerprint Dive into the research topics of 'Triggering receptor expressed on myeloid cells-2 is involved in prion-induced microglial activation but does not contribute to prion pathogenesis in mouse brains'. Together they form a unique fingerprint.

Cite this