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Identifier 000457355
Title Assessing the role of microglial autophagy in immune responses in the EAE model of Multiple Sclerosis
Alternative Title Διερεύνηση του ρόλου της αυτοφαγίας στη μικρογλοία κατά την επαγωγή ανοσολογικών αποκρίσεων στο μοντέλο ΕΑΕ της Σκλήρυνσης κατά Πλάκας
Author Ξανθοπούλου, Δέσποινα
Thesis advisor Βεργίνης, Παναγιώτης
Reviewer Τσατσάνης Χρήστος
Χαραλαμπόπουλος, Ιωάννης
Abstract Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is the most commonly used animal model to study the autoimmune inflammatory phase of MS. In MS there is infiltration and reactivation of peripheral CD4+ T cells and CD8+ T cells and their dispersion into the CNS parenchyma. Microglia are the most abundant mononuclear phagocytes in the CNS and make up the principal resident immune cells of the brain. Microglia are highly involved in homeostasis and in host defence against pathogens and CNS disorders. Microglia also have the lysosomal machinery required for processing and presentation of antigenic peptides. In early phases of MS activated microglia can damage oligodendrocytes and neurons directly by releasing harmful factors or indirectly by secreting pro- inflammatory cytokines, that propagate inflammation and leukocyte infiltration. However, microglia perform beneficial roles especially during remission phase of MS since they can clean up myelin debris and enhance tissue repair. Autophagy is a lysosomal degradation system that is connected to MS progression. Microglial autophagy is essential for the clearance of myelin debris and is implicated in the regulation of microglial inflammation and antigen presentation capacity. Preliminary data from our lab demonstrated that conditional ablation of Atg5 transcript in microglial cells resulted in amelioration of EAE which can be attributed to the significant accumulation of Tregs and MDSCs in the spinal cord. Nevertheless, we faced technical challenges regarding disease induction and reaching the desirable clinical. With in vitro studies, we observed that inflammatory stimuli, such as LPS, and cytokines (IFNγ and IFNα) influence differently the microglial autophagic machinery. Finally, we validated with immunofluorescence the Atg5 ablation and confirmed that ATG5 is an essential regulator of autophagy since it prevented IFNγ-driven autophagy induction.
Language English
Subject Microglia
Αυτοφαγία
Issue date 2023-07-28
Collection   School/Department--School of Medicine--Department of Medicine--Post-graduate theses
  Type of Work--Post-graduate theses
Permanent Link https://elocus.lib.uoc.gr//dlib/e/9/4/metadata-dlib-1689669834-454886-28944.tkl Bookmark and Share
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