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

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...

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Veröffentlicht in:Neurobiology of aging 2015-05, Vol.36 (5), p.1994-2003
Hauptverfasser: Zhu, Caihong, Herrmann, Uli S, Li, Bei, Abakumova, Irina, Moos, Rita, Schwarz, Petra, Rushing, Elisabeth J, Colonna, Marco, Aguzzi, Adriano
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Sprache:eng
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Zusammenfassung: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.
ISSN:0197-4580
1558-1497
1558-1497
DOI:10.1016/j.neurobiolaging.2015.02.019