Autophagy: a Novel Pathway of Antigen Presentation in Dendritic Cells

Project Details

Autophagy is a critical cellular pathway with important implications for human disease. Specifically, autophagy is the trafficking of cytoplasmic content to lysosomal compartments where it is degraded. Initially described as a process induced only in nutrient-deprived cells, autophagy is now known to occur constitutively in many cell types, including dendritic cells (DC). DC play a pivotal role in innate and acquired immunity. Autophagy is implicated in DC detection of microbial products, phagosome-lysosome fusion and antigen trafficking for MHC class II (MHCII) presentation. Consequently, autophagy has major implications for DC biology in disease scenarios, such as infectious pathogen clearance and/or autoimmunity. Autophagy in DC function is an emerging field of research that has not been extensively investigated. To date, autophagy participation in specific DC subsets is unknown, its contribution to MHC class I (MHCI) antigen presentation is under studied and only limited analysis of autophagy during in vivo viral infection has been undertaken. Given our expertise in isolation of rare DC subsets, study of antigen presentation pathways and mouse models of viral infection we are in a unique position to examine autophagy as a novel pathway in DC. Proteomics, high-resolution microscopy.

Researchers

Professor Jose Villadangos

Collaborators

Dr Justine Mintern

Research Publications

Mintern JD, Villadangos JA.  Autophagy and mechanisms of effective immunity. Frontiers in Immunology 2012; 3: 60.

Mintern JD, Macri C, Chin WJ, Panozza SE, Segura E, Patterson NL, Zeller P, Bourges D, Bedoui S, McMillan PJ, Idris A, Nowell CJ, Brown A, Radford K, Johnston APR, Villadangos JA.  Differential use of autophagy by primary dendritic cells specialised in cross-presentation. Autophagy 2015; 11: 906-917.

Mintern JD, Macri C, Villadangos JA.  Modulation of antigen presentation by intracellular trafficking. Curr Opin Immunol 2015; 34: 16-21.