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LC3 associated phagocytosis

Gholamreza Fazeli, Michaela Trinkwalder, Linda Irmisch, Ann Marie Wehman
In animals, the midbody coordinates the end of cytokinesis when daughter cells separate through abscission. The midbody was thought to be sequestered by macroautophagy, but recent evidence suggests that midbodies are primarily released and phagocytosed. It was unknown, however, whether autophagy proteins play a role in midbody phagosome degradation. Using a protein degradation assay, we show that midbodies are released in Caenorhabditis elegans Released midbodies are known to be internalized by actin-driven phagocytosis, which we show requires the RAB-5 GTPase to localize the class III phosphoinositide 3-kinase (PI3K) complex at the cortex...
October 15, 2016: Journal of Cell Science
Marija Cemma, Sergio Grinstein, John H Brumell
Phagocytosis plays a central role in immunity and tissue homeostasis. After internalization of cargo into single-membrane phagosomes, these compartments undergo a maturation sequences that terminates in lysosome fusion and cargo degradation. Components of the autophagy pathway have recently been linked to phagosome maturation in a process called LC3-associated phagocytosis (LAP). In this process, autophagy machinery is thought to conjugate LC3 directly onto the phagosomal membrane to promote lysosome fusion...
September 2016: Autophagy
Urmi Bandyopadhyay, Michael Overholtzer
The autophagy-related process LC3-Associated Phagocytosis, or LAP, is known to control the degradation of engulfed cells and microorganisms. Now Martinez et al. discover that LAP controls immune responses to dying cells and its inhibition leads to development of Systemic Lupus Erythematosus-like disease.
August 2016: Cell Research
Christine Matte, Pierre-André Casgrain, Olivier Séguin, Neda Moradin, Wan Jin Hong, Albert Descoteaux
The protozoan Leishmania parasitizes macrophages and evades the microbicidal consequences of phagocytosis through the inhibition of phagolysosome biogenesis. In this study, we investigated the impact of this parasite on LC3-associated phagocytosis, a non-canonical autophagic process that enhances phagosome maturation and functions. We show that whereas internalization of L. major promastigotes by macrophages promoted LC3 lipidation, recruitment of LC3 to phagosomes was inhibited through the action of the parasite surface metalloprotease GP63...
June 2016: PLoS Pathogens
Rachasak Boonhok, Nattawan Rachaphaew, Apisak Duangmanee, Pornpimol Chobson, Sittiporn Pattaradilokrat, Pongsak Utaisincharoen, Jetsumon Sattabongkot, Marisa Ponpuak
IFN-γ is a major regulator of immune functions and has been shown to induce liver-stage Plasmodium elimination both in vitro and in vivo. The molecular mechanism responsible for the restriction of liver-stage Plasmodium downstream of IFN-γ remains uncertain, however. Autophagy, a newly described immune defense mechanism, was recently identified as a downstream pathway activated in response to IFN-γ in the control of intracellular infections. We thus hypothesized that the killing of liver-stage malarial parasites by IFN-γ involves autophagy induction...
June 21, 2016: Proceedings of the National Academy of Sciences of the United States of America
Evelien G G Sprenkeler, Mark S Gresnigt, Frank L van de Veerdonk
LC3-associated phagocytosis (LAP) is a non-canonical autophagy pathway involved in the maturation of single-membrane phagosomes and subsequent killing of ingested pathogens by phagocytes. This pathway is initiated following recognition of pathogens by pattern recognition receptors and leads to the recruitment of LC3 into the phagosomal membrane. This form of phagocytosis is utilized for the antifungal host defence and is required for an efficient fungal killing. Here, we provide an overview of the LAP pathway and review the role of LAP in anti-Aspergillus host defence, as well as mechanisms induced by Aspergillus that modulate LAP to promote its survival in the host...
September 2016: Cellular Microbiology
Jennifer Martinez, Larissa D Cunha, Sunmin Park, Mao Yang, Qun Lu, Robert Orchard, Quan-Zhen Li, Mei Yan, Laura Janke, Cliff Guy, Andreas Linkermann, Herbert W Virgin, Douglas R Green
Defects in clearance of dying cells have been proposed to underlie the pathogenesis of systemic lupus erythematosus (SLE). Mice lacking molecules associated with dying cell clearance develop SLE-like disease, and phagocytes from patients with SLE often display defective clearance and increased inflammatory cytokine production when exposed to dying cells in vitro. Previously, we and others described a form of noncanonical autophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles, including dying cells, recruit elements of the autophagy pathway to facilitate maturation of phagosomes and digestion of their contents...
May 5, 2016: Nature
Jenny M Tam, Michael K Mansour, Mridu Acharya, Anna Sokolovska, Allison K Timmons, Adam Lacy-Hulbert, Jatin M Vyas
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)...
2016: Pathogens
Georgios Chamilos, Tonia Akoumianaki, Irene Kyrmizi, Axel Brakhage, Anne Beauvais, Jean-Paul Latge
Intracellular swelling of conidia of the major human airborne fungal pathogen Aspergillus fumigatus results in surface exposure of immunostimulatory pathogen-associated molecular patterns (PAMPs) and triggers activation of a specialized autophagy pathway called LC3-associated phagocytosis (LAP) to promote fungal killing. We have recently discovered that, apart from PAMPs exposure, cell wall melanin removal during germination of A. fumigatus is a prerequisite for activation of LAP. Importantly, melanin promotes fungal pathogenicity via targeting LAP, as a melanin-deficient A...
May 3, 2016: Autophagy
D R Green, T H Oguin, J Martinez
Phagocytic cells of the immune system must constantly survey for, recognize, and efficiently clear the billions of cellular corpses that arise as a result of development, stress, infection, or normal homeostasis. This process, termed efferocytosis, is critical for the prevention of autoimmune and inflammatory disorders, and persistence of dead cells in tissue is characteristic of many human autoimmune diseases, notably systemic lupus erythematosus. The most notable characteristic of the efferocytosis of apoptotic cells is its 'immunologically silent' response...
June 2016: Cell Death and Differentiation
Masashi Kanayama, Keiko Danzaki, You-Wen He, Mari L Shinohara
Recruiting pathogenic T cells to the central nervous system (CNS) is a critical step during the development of experimental autoimmune encephalomyelitis (EAE). Here, we report that the absence of autophagy and microtubule-associated protein 1A/1B-light chain 3-associated phagocytosis significantly delayed the onset of EAE in Atg7 conditional knockout (Atg7 CKO) mice in myeloid cells. T-helper cell-cell priming appeared to be normal in the Atg7 CKO mice, but the mice showed significant accumulation of Th17 cells in the lung...
September 2016: International Immunology
Masashi Kanayama, Mari L Shinohara
Autophagy was initially characterized as a process to digest cellular components, including damaged cell organelles or unused proteins. However, later studies showed that autophagy plays an important role to protect hosts from microbial infections. Accumulating evidences showed the contribution of autophagy itself and autophagy-related proteins (ATGs) in the clearance of bacteria, virus, and parasites. A number of studies also revealed the molecular mechanisms by which autophagy is initiated and developed. Furthermore, it is now understood that some ATGs are shared between two distinct processes; autophagy and LC3-associated phagocytosis (LAP)...
2016: Frontiers in Immunology
Ming Shi, Yifan Zhang, Leyuan Liu, Tingting Zhang, Fang Han, Joseph Cleveland, Fen Wang, Wallace L McKeehan, Yu Li, Dekai Zhang
Phagocytosis is a critical cellular process for innate immune defense against microbial infection. The regulation of phagocytosis process is complex and has not been well defined. An intracellular molecule might regulate cell surface-initiated phagocytosis, but the underlying molecular mechanism is poorly understood (1). In this study, we found that microtubule-associated protein 1S (MAP1S), a protein identified recently that is involved in autophagy (2), is expressed primarily in macrophages. MAP1S-deficient macrophages are impaired in the phagocytosis of bacteria...
January 15, 2016: Journal of Biological Chemistry
Craig R Brooks, Melissa Y Yeung, Yang S Brooks, Hui Chen, Takaharu Ichimura, Joel M Henderson, Joseph V Bonventre
Phagocytosis of apoptotic cells by both professional and semi-professional phagocytes is required for resolution of organ damage and maintenance of immune tolerance. KIM-1/TIM-1 is a phosphatidylserine receptor that is expressed on epithelial cells and can transform the cells into phagocytes. Here, we demonstrate that KIM-1 phosphorylation and association with p85 results in encapsulation of phagosomes by lipidated LC3 in multi-membrane organelles. KIM-1-mediated phagocytosis is not associated with increased ROS production, and NOX inhibition does not block LC3 lipidation...
October 1, 2015: EMBO Journal
Dah-Shyong Yu, Chia-Lun Wu, Szu-Yuan Ping, Cheng Keng, Kun-Hung Shen
Immunotherapy using bacille Calmette-Guerin (BCG) instillation is the mainstay treatment modality for superficial urothelial cancer (UC) through toll-like receptor (TLR) activation of cognitive immune response. We investigated the roles of TLR7 in the activation of apoptosis in UC cells after BCG treatment. The in vitro cytotoxicity effect of BCG on UC cells was measured by a modified 3-(4,5-dimethylthiazo-2-yl)-2,5-diphenyl tetrazolium assay. Expressions of TLR7 mRNA and protein in native UC cells prior to and after BCG treatment were analyzed using real-time quantitative polymerase chain reaction and western blot methods...
August 2015: Kaohsiung Journal of Medical Sciences
Keith B Boyle, Felix Randow
Phagocytic cells engulf their prey into vesicular structures called phagosomes, of which a certain proportion becomes demarcated for enhanced maturation by a process called LC3-associated phagocytosis (LAP). Light has now been shed on the molecular requirements of LAP, establishing a central role for the protein Rubicon in the immune response to Aspergillus fumigatus.
July 2015: Nature Cell Biology
Jennifer Martinez, R K Subbarao Malireddi, Qun Lu, Larissa Dias Cunha, Stephane Pelletier, Sebastien Gingras, Robert Orchard, Jun-Lin Guan, Haiyan Tan, Junmin Peng, Thirumala-Devi Kanneganti, Herbert W Virgin, Douglas R Green
LC3-associated phagocytosis (LAP) is a process wherein elements of autophagy conjugate LC3 to phagosomal membranes. We characterize the molecular requirements for LAP, and identify Rubicon as being required for LAP but not autophagy. Rubicon is recruited to LAPosomes and is required for the activity of a Class III PI(3)K complex containing UVRAG but lacking ATG14 and Ambra1. This allows for the sustained localization of PtdIns(3)P, which is critical for recruitment of downstream autophagic proteins and stabilization of the NOX2 complex to produce reactive oxygen species...
July 2015: Nature Cell Biology
François-Xavier Campbell-Valois, Martin Sachse, Philippe J Sansonetti, Claude Parsot
UNLABELLED: The enteropathogenic bacterium Shigella flexneri uses a type 3 secretion apparatus (T3SA) to transfer proteins dubbed translocators and effectors inside host cells, inducing bacterial uptake and subsequent lysis of the entry vacuole. Once in the cytoplasm, the outer membrane protein IcsA induces actin polymerization, enabling cytoplasmic movement and cell-to-cell spread of bacteria. During this infectious process, S. flexneri is targeted by ATG8/LC3. The effector IcsB was proposed to inhibit LC3 recruitment by masking a region of IcsA recognized by the autophagy pathway component ATG5...
2015: MBio
Christian Münz
Macroautophagy delivers cytoplasmic constituents for lysosomal degradation. Because MHC class II molecules are loaded with lysosomal products for CD4(+) T-cell stimulation, macroautophagy supports intracellular antigen processing onto MHC class II molecules. The molecular machinery of macroautophagy, however, does not only support this autophagic antigen processing, but seems to also modify extracellular antigen uptake for MHC class II presentation, antigen exocytosis, and packaging for improved cross-presentation onto MHC class I molecules...
2015: Frontiers in Immunology
Nadia S Deen, Lan Gong, Thomas Naderer, Rodney J Devenish, Terry Kwok
BACKGROUND: Previous findings have suggested that Helicobacter pylori induces autophagic processes and subsequently takes refuge in autophagosomes, thereby contributing to persistent infection. Recently, a noncanonical form of autophagy, LC3 (microtubule-associated protein 1 light chain 3)-associated phagocytosis (LAP), has been shown to be required for efficient clearance of some intracellular bacteria. Whether H. pylori infection induces LAP had not been examined previously. In this study, we determined the extent to which H...
December 2015: Helicobacter
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