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Pathogens 2016, 5(2), 34;

The Role of Autophagy-Related Proteins in Candida albicans Infections

Department of Medicine, Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA
Immunology Program, Benaroya Research Institute, Seattle, WA 98101, USA
Author to whom correspondence should be addressed.
Academic Editors: Gianfranco Donelli and Bernhard Hube
Received: 27 January 2016 / Revised: 26 February 2016 / Accepted: 22 March 2016 / Published: 29 March 2016
(This article belongs to the Special Issue Candida Albicans Infections)
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Autophagy plays an important role in maintaining cell homeostasis by providing nutrients during periods of starvation and removing damaged organelles from the cytoplasm. A marker in the autophagic process is the reversible conjugation of LC3, a membrane scaffolding protein, to double membrane autophagosomes. Recently, a role for LC3 in the elimination of pathogenic bacteria and fungi, including Candida albicans (C. albicans), was demonstrated, but these organisms reside in single membrane phagosomes. This process is distinct from autophagy and is termed LC3-associated phagocytosis (LAP). This review will detail the hallmarks of LAP that distinguish it from classical autophagy and review the role of autophagy proteins in host response to C. albicans and other pathogenic fungi. View Full-Text
Keywords: autophagy; LC3-associated phagocytosis (LAP); Candida albicans; Aspergillus fumigatus; LC3; innate immunity; Dectin-1 autophagy; LC3-associated phagocytosis (LAP); Candida albicans; Aspergillus fumigatus; LC3; innate immunity; Dectin-1

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Tam, J.M.; Mansour, M.K.; Acharya, M.; Sokolovska, A.; Timmons, A.K.; Lacy-Hulbert, A.; Vyas, J.M. The Role of Autophagy-Related Proteins in Candida albicans Infections. Pathogens 2016, 5, 34.

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