128 Chapter 5 endothelial cells may contribute to TSPO signal in other conditions. Overall, these results confirm the complexity of TSPO and show the necessity to validate their cellular origin in each pathological context before quantifying and interpreting the in vivo imaging signal. Conclusion Since its identification, TSPO has beenwidely studied for its different roles in the periphery and more recently within the CNS itself. Its cellular origin demonstrated in the brain in microglia, although it is clear that other cell types also express TSPO and its presence in astrocytes and endothelial cells is now well accepted (Fig. 1). The cellular origin of TSPO alterations likely not only depends on the pathology but also on the developmental stage and mode of cell activation. Monitoring of TSPO levels is now widely used as a marker of inflammation, but research still needs to better characterize the means and cells involved. In this sense, it has recently been reported that the expression of TSPO concerns not only the pro-inflammatory types of microglia but also the anti-inflammatory subtypes. Future studies should also reveal the therapeutic potential of a change in its levels. Acknowledgements Authors thank theMS society of Great Britain and Northern Ireland. Authors K.C. and B.B.T. are supported by the Velux foundation (project n. 1123). Author S.T. received support from the Swiss National Science Foundation (Early PostDoc.Mobility Scholarship, no. P2GEP3_191446), the Prof Dr Max Cloëtta Foundation (Clinical Medicine Plus scholarship) and the Jean and Madeleine Vachoux Foundation. Author D.R.O. is supported by the MRC (MR/N008219/1). Author V.P. was supported by the John Stauffer Dean’s Chair in Pharmaceutical Sciences (University of Southern California). This work was supported by the Swiss National Science Foundation (no. 320030-184713).
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