TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration

Nat Neurosci. 2022 Jan;25(1):26-38. doi: 10.1038/s41593-021-00975-6. Epub 2021 Dec 16.

Abstract

Triggering receptor expressed on myeloid cell 2 (TREM2) is linked to risk of neurodegenerative disease. However, the function of TREM2 in neurodegeneration is still not fully understood. Here, we investigated the role of microglial TREM2 in TAR DNA-binding protein 43 (TDP-43)-related neurodegeneration using virus-mediated and transgenic mouse models. We found that TREM2 deficiency impaired phagocytic clearance of pathological TDP-43 by microglia and enhanced neuronal damage and motor impairments. Mass cytometry analysis revealed that human TDP-43 (hTDP-43) induced a TREM2-dependent subpopulation of microglia with high CD11c expression and phagocytic ability. Using mass spectrometry (MS) and surface plasmon resonance (SPR) analysis, we further demonstrated an interaction between TDP-43 and TREM2 in vitro and in vivo as well as in human tissues from individuals with amyotrophic lateral sclerosis (ALS). We computationally identified regions within hTDP-43 that interact with TREM2. Our data highlight that TDP-43 is a possible ligand for microglial TREM2 and that this interaction mediates neuroprotection of microglia in TDP-43-related neurodegeneration.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • DNA-Binding Proteins* / genetics
  • DNA-Binding Proteins* / metabolism
  • Membrane Glycoproteins* / genetics
  • Membrane Glycoproteins* / metabolism
  • Mice
  • Mice, Transgenic
  • Microglia* / metabolism
  • Neurodegenerative Diseases* / metabolism
  • Neuroprotection
  • Receptors, Immunologic* / genetics
  • Receptors, Immunologic* / metabolism

Substances

  • DNA-Binding Proteins
  • Membrane Glycoproteins
  • Receptors, Immunologic
  • TDP-43 protein, mouse
  • Trem2 protein, mouse