Résumé :
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More and more experiments show the role of immune cells and immunological molecules in the physiology of the nervous system including neurogenesis. A better knowledge of interactions between immune cells and neural stem cells is important for improving and controlling the capacity of either endogenous or grafted adult neural stem cells to repair the nervous system. We address the question of the role of Major Histocompatibility Complex-I (MHC-I) molecules in neurogenesis in the mouse model. Our main results concern the expression and functions of Rae-1, a molecule related to the MHC-I family. Rae-1 was expressed by neural stem cells and was down regulated after their differentiation. Rae-1 transcripts were known to be present only in early embryonic stages particularly in the nervous tissue. Moreover, we showed that Rae-1 was also expressed in the regions of adult neurogenesis and its expression was induced in the olfactory bulbs after olfactory axotomy. Rae-1 is recognized by NKG2D, the main activator receptor of the NK, NKT and T ?? lymphocytes. In the model of olfactory axotomy, we demonstrated a recruitment of lymphocytes in the olfactory bulbs which correlated with an increase in NKG2D transcripts. However, no NKG2D expression was detected in the subventricular zone in physiological or pathological condition. We thus questioned a role of Rae-1 in the absence of immune cells. Using a transduction approach with lentivirus coding for shRNAs targeting Rae-1, we demonstrated that Rae-1 is involved in the proliferation of neural stem cells. Deciphering the roles in vivo of Rae-1 in neurogenesis is now our main objective.
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