Immunoamphisomes in dendritic cells amplify TLR signaling and enhance exogenous antigen presentation on MHC-II.
Autophagy, a specialized lysosomal degradation pathway, has proven to be a potent cell-autonomous defense mechanism against a range of intracellular microbes. In addition, autophagy emerged recently as a critical regulator of innate and adaptive immune responses. Links between autophagy and innate immunity are being progressively unveiled. For instance, several TLR (Toll-like receptor) agonists upregulate autophagy flux in immune cell types such as DC (dendritic cells) or macrophages. Conversely, and perhaps surprisingly, is the observation that TLR7-mediated responses might depend on autophagy in plasmacytoid DC, thus suggesting a more complex link between TLR-dependent responses and autophagy. Recently, the demonstration that NOD2 increases autophagy suggests that innate immune responses initiated via a broad range of pathogen recognition receptors can regulate autophagy. In addition to its involvement in innate immune responses, autophagy regulates adaptive immune responses via both MHC class I and class II molecules depending on the cellular context and the nature of the antigen.
Blanchet
Fabien P
FP
Departments of Dermatology and Venereology, Microbiology and Molecular Medicine, University Hospital and Medical School of Geneva, Geneva, Switzerland.
Piguet
Vincent
V
D000818:Animals; D017951:Antigen Presentation / Q000276:immunology*; D001343:Autophagy / Q000276:immunology; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D018448:Models, Immunological; D010588:Phagosomes / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology*
D000949:Histocompatibility Antigens Class II; D051193:Toll-Like Receptors