Contributions
Abstract: P961
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models
Retinoic acid early induced transcript-1 (RAE-1) glycoproteins are stress molecules and ligands of the activating immune receptor NKG2D expressed by Natural Killer cells and cytotoxic CD8 T cell infiltrating CNS during experimental autoimmune encephalomyelitis (EAE). We showed that Raet1 transcripts are induced in the spinal cord in EAE model which is accompanied by microglia proliferation and activation, recruitment of immune cells and neurogenesis. We herein studied the time course expression of the two members of the Raet1 gene family present in C57BL/6 mice, namely Raet1d and Raet1e, in the spinal cord during EAE. We report that Raet1d and Raet1e genes are induced early upon EAE onset and reach a maximal expression at the peak of the pathology. We show that myeloid cells, i.e. macrophages as well as microglia, are cellular sources of Raet1 transcripts. We also demonstrate that only Raet1d expression is induced in microglia, whereas macrophages expressed both Raet1d and Raet1e. Furthermore, we investigated the dynamics of RAE-1 expression in microglia cultures. RAE-1 induction correlated with cell proliferation but not with M1/M2 phenotypic orientation. We finally demonstrate that macrophage colony-stimulating factor (M-CSF) is a major factor controlling RAE-1 expression in microglia.
Disclosure: Nothing to disclose
Abstract: P961
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models
Retinoic acid early induced transcript-1 (RAE-1) glycoproteins are stress molecules and ligands of the activating immune receptor NKG2D expressed by Natural Killer cells and cytotoxic CD8 T cell infiltrating CNS during experimental autoimmune encephalomyelitis (EAE). We showed that Raet1 transcripts are induced in the spinal cord in EAE model which is accompanied by microglia proliferation and activation, recruitment of immune cells and neurogenesis. We herein studied the time course expression of the two members of the Raet1 gene family present in C57BL/6 mice, namely Raet1d and Raet1e, in the spinal cord during EAE. We report that Raet1d and Raet1e genes are induced early upon EAE onset and reach a maximal expression at the peak of the pathology. We show that myeloid cells, i.e. macrophages as well as microglia, are cellular sources of Raet1 transcripts. We also demonstrate that only Raet1d expression is induced in microglia, whereas macrophages expressed both Raet1d and Raet1e. Furthermore, we investigated the dynamics of RAE-1 expression in microglia cultures. RAE-1 induction correlated with cell proliferation but not with M1/M2 phenotypic orientation. We finally demonstrate that macrophage colony-stimulating factor (M-CSF) is a major factor controlling RAE-1 expression in microglia.
Disclosure: Nothing to disclose