Phenotyping TREM2+ cells in postnatal C57/Bl6 mice brain

CHERTOFF, MARIELA; SHRIVASTAVA KALPANA; ACARIN LAIA; GIMENEZ LLORT LYDIA

Simposio; The 3rd Venusberg Meeting on Neuroinflammation; 2013

The lost-of-function of Triggering Receptor Expressed on Myeloid cells 2 (TREM2) or its coreceptor DAP12 are responsible for the recessively inherited Nasu-Hakola disease (also known as PLOSL). The brains of PLOSL affected patients show strong microglial activation in the cerebral white matter. In rodent CNS, TREM2 is mainly express in microglia, but it has been described also in neurons. The expression of TREM2 in olgodendrocytes is still controversial. Recently, variants or mutations of TREM2 has been associated with Frontotemporal Dementia-like Syndrome, Early onset Dementia, Alzheimer´s Disease. Due to little is known about the postnatal distribution of TREM2, the aim of this study is to analyze the phenotype of TREM2+ cells during postnatal day 1 to 10 in C57/Bl6 mice brain. Immunohistochemistry for TREM2 was performed to study the distribution of its expression in postnatal brain. Double or triple immunofluorescence were performed for several markers of astrocytes, oligodendrocytes and microglia in order to phenotype the TREM2+ cells. Confocal images were analyzed in order to confirm colocalization. Our results shown that TREM2 is mainly express in  cortex and white matter at P1 and in neuroephitelium from P1 to P7. In P10 mice, TREM2 is only present in corpus callosum and disappear after P12 in our mice. No colocalization of TREM2 with oligodendrocyte markers has been found at any time-point studied. Interestingly, we observed that TREM2+ microglia in postnatal brain express also markers of alternative activation, such as Arginase-1 and CD206.