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Le rôle des protéines à ancre GPI chez Candida albicans dans les interactions hote/pathogène

Abstract : Candida albicans is the fungal pathogen isolated most frequently in nosocomial infections and in hemocultures. Our proposal in this thesis was to extend our knowledge on one particular class of cell surface proteins: GPI (Glycosyl Phospho Inositol)-anchored proteins (GpiP). Gpi7p has been demonstrated by our group to participate in the proper anchoring of GPI-dependent cell wall proteins to the cell wall and also suggested that GPI anchored proteins (GAP) might be involved in macrophage interactions especially in fungal survival after phagocytosis. In the C. albicans genome, 104 putative GPI anchored proteins have been identified but the role of about half of them remains unknown. These observations altogether suggest that GAPs might be excellent targets to study host-pathogen interactions. For this study we used two approaches. The first strategy was to generate null mutants of the putative GPI anchored proteins, then characterize their phenotype in vitro and finally screen each of the mutants for its interaction with macrophages. This global approach was conducted on the 47 mutants gathered and permitted us to classify GAPs in three main functional categories: (i) morphogenesis, (ii) stress response and (iii) cell wall integrity and caspofungin sensitivity. The screen for mutant altered in their resistance to phagocytosis did not give any clear results, probably because the conditions tested were too mild. In the second approach, we used the mutant gpi7-/- to study the effects of some cell wall proteins mislocalisation in the interaction of the fungus with the innate host defences. We found that in the absence of Gpi7p, C. albicans elicited a stronger in vitro TNF-Α production by macrophages and a stronger recruitment of neutrophils in vivo at the site of infection. These findings suggest the strongly modified cell wall of gpi7-/- is better recognized by the immune system inducing a stronger proinflammatory response. None of these effects seem to be mediated by the TLR2 and TLR4 receptors.
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Contributor : Jean-Marie Beckerich <>
Submitted on : Thursday, February 15, 2007 - 12:59:08 PM
Last modification on : Tuesday, March 17, 2020 - 1:38:51 AM
Long-term archiving on: : Tuesday, April 6, 2010 - 10:32:55 PM


  • HAL Id : tel-00131148, version 1



Armêl Plaine. Le rôle des protéines à ancre GPI chez Candida albicans dans les interactions hote/pathogène. Biologie cellulaire. Institut national agronomique paris-grignon - INA P-G, 2006. Français. ⟨tel-00131148⟩



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