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Published on: April 13, 2017
Triggering receptor expressed on myeloid cells-2 is involved in prion-induced microglial activation but does not
Caihong Zhu1, Uli S Herrmann1, Bei Li1
1Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland.
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.
Insights
Triggering receptor expressed on myeloid cells-2 (TREM2) is implicated in neurodegeneration. While TREM2 influences microglial activation in prion disease models, it does not alter disease progression or survival.
Area of Science:
- Neuroimmunology
- Neurodegenerative Diseases
- Prion Biology
Background:
- Dysfunctional variants of TREM2 (triggering receptor expressed on myeloid cells-2) are linked to Alzheimer's and other neurodegenerative diseases.
- Microglia, the brain's immune cells, play a critical role in neuroinflammation and disease pathogenesis.
Purpose of the Study:
- To investigate the role of TREM2 in the context of prion disease.
- To determine if TREM2 influences microglial activation and disease progression in experimental prion infections.
Main Methods:
- Analysis of TREM2 expression in microglia during prion infection.
- Assessment of disease incubation time and survival in TREM2-deficient (TREM2(-/-)) mice infected with prions.
- Profiling of microglial activation markers and phenotypes in prion-infected TREM2(-/-) mice.
Main Results:
- TREM2 expression was significantly upregulated in microglia upon prion infection.
- Depletion of TREM2 did not impact disease incubation time or survival.
- Markers of microglial activation were attenuated in prion-infected TREM2(-/-) mice.
- TREM2 deficiency did not alter overall microglial phenotypes.
Conclusions:
- TREM2 is involved in modulating prion-induced microglial activation.
- TREM2 does not significantly affect the overall pathogenesis or progression of experimental prion infections.
