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Étude de l'implication d’une voie MyD88/IL-22 dans le contrôle de la colonisation par la bactérie segmentée filamenteuse

Abstract : The mammalian intestine is heavily colonized by a huge microbial community. During a long coevolution process, the host has evolved mutualistic relationships with its microbiota. Thes relationships, mainly based on metabolstic advantages, also allow the full maturation of the host immune system, which development is initiated in utero by a genetic program. In mice, only SFB has been yet described to display strong immunostimulant properties allowing the coordination of a large panel of immune responses, more specifically IgA and Th17 responses, which preferential induction sites might be the Peyer's patches. The first part of my thesis contributed to complete a work dedicated to the characterization of the IgA et Th17 responses induced by SFB. We have underscored SFB capacity to stimulate the post-natal maturation of isolated lymphoid follicles and also tertiary lymphoid tissues that would substitute to Peyer's patches as inductors sites of both IgA and Th17 responses induced by SFB. However, this microbiote also constitutes a potential antigenic threat for the host integrity. Notably, the SFB could provoke chronic deleterious inflammation in peripheric compartment in genetically predisposed individuals. It suggests the establishment of highly regulated mechanisms regulating SFB colonization, to avoid compromising events for the host homeostasis. In a second part of my thesis, with the help of immunodeficient axenic mice, we have shown a role of TLR signaling pathways in the control of SFB colonization. However, antimicrobial peptides, IgA, IL-17 or IL-22 seem to be involved int eh control of SFB colonization.
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Submitted on : Saturday, February 1, 2020 - 1:02:12 AM
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Marion Picard. Étude de l'implication d’une voie MyD88/IL-22 dans le contrôle de la colonisation par la bactérie segmentée filamenteuse. Immunologie. Université Sorbonne Paris Cité, 2017. Français. ⟨NNT : 2017USPCB107⟩. ⟨tel-02463458⟩



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