About this Research Topic
Phagocytosis is a universal cell function, which starts with the recognition and binding of a particle (over 0.5 μm in diameter), generally in a receptor-dependent manner, and leads to its internalization and degradation. Single-celled eukaryotes, such as the mold Dictyostelium discoideum and amoebae, use phagocytosis for feeding. In higher eukaryotes, the phagocytes of the immune system, including neutrophils, macrophages, monocytes and dendritic cells, have been extensively investigated for their role in anti-microbial defense. Their emerging roles in the removal of apoptotic, necrotic or cancer cells has extended the interest in their function beyond host defense, and they are now considered as key keepers of tissue homeostasis and remodeling.
The functional diversity of phagocytes is determined by their plasticity. Different types of phagocytes had been defined, including pro-inflammatory or anti-inflammatory macrophages and neutrophils, and tumor associated macrophages and neutrophils (TAM and TAN). Often, these sub-populations display differential expression of phagocytic receptors, which may determine the type of particle to be phagocytized. Receptors with phagocytic activity are: pathogen-associated molecular patterns receptors, apoptotic receptors, patterns of endogenous danger receptors and the opsono-phagocytic receptors. In addition, other receptors expressed in phagocytes cooperate in particle recognition and in the modulation of phagocytosis.
Independently of the nature of the particle to be engulfed, innate immune phagocytes eliminate their targets mainly by phagocytosis. Phagocytosis is a complex multistep and multiplex process whereby cells engulf particles of different nature, shapes and sizes and react to their mechanical properties. This whole process requires multiple and highly coordinated events including receptor priming, membrane remodeling, fine-tuned actin cytoskeleton rearrangements, vesicle trafficking, phagosome formation and maturation, all of which culminate in the elimination of the target particle. In virtue of this complexity, a myriad of intracellular signaling molecules and contractile proteins are required to resolve the different steps of the process. Each step is tightly regulated and in many cases, the molecules involved can be quite different depending on the type of receptor implicated in phagocytosis.
The goals of this Research Topic are to provide an overview of the molecular mechanisms controlling phagocytosis with respect to the immune system as well as the different physiological settings in which phagocytosis is involved. We welcome the submission of articles that cover, but are not limited to, the following sub-topics:
1. Signaling pathways regulated by phagocytic receptors in immune cells (CR3/CR4, FcγR, Dectin, DC-SIGN, scavenger receptors)
2. Actin cytoskeleton dynamics during phagocytosis and its implications for phagocytic functions.
3. Molecular processes involved in phagosome formation and sealing in phagocytic cells of the immune system.
4. Vesicular trafficking.
5. Phagocytosis of bacterial, fungal and parasitic pathogens.
6. Phagocytosis and antigen presentation.
7. Phagocytosis of apoptotic cells and resolution of inflammation.
8. Phagocytosis of cancer cells in the context of anti-tumor immunity.
The functional diversity of phagocytes is determined by their plasticity. Different types of phagocytes had been defined, including pro-inflammatory or anti-inflammatory macrophages and neutrophils, and tumor associated macrophages and neutrophils (TAM and TAN). Often, these sub-populations display differential expression of phagocytic receptors, which may determine the type of particle to be phagocytized. Receptors with phagocytic activity are: pathogen-associated molecular patterns receptors, apoptotic receptors, patterns of endogenous danger receptors and the opsono-phagocytic receptors. In addition, other receptors expressed in phagocytes cooperate in particle recognition and in the modulation of phagocytosis.
Independently of the nature of the particle to be engulfed, innate immune phagocytes eliminate their targets mainly by phagocytosis. Phagocytosis is a complex multistep and multiplex process whereby cells engulf particles of different nature, shapes and sizes and react to their mechanical properties. This whole process requires multiple and highly coordinated events including receptor priming, membrane remodeling, fine-tuned actin cytoskeleton rearrangements, vesicle trafficking, phagosome formation and maturation, all of which culminate in the elimination of the target particle. In virtue of this complexity, a myriad of intracellular signaling molecules and contractile proteins are required to resolve the different steps of the process. Each step is tightly regulated and in many cases, the molecules involved can be quite different depending on the type of receptor implicated in phagocytosis.
The goals of this Research Topic are to provide an overview of the molecular mechanisms controlling phagocytosis with respect to the immune system as well as the different physiological settings in which phagocytosis is involved. We welcome the submission of articles that cover, but are not limited to, the following sub-topics:
1. Signaling pathways regulated by phagocytic receptors in immune cells (CR3/CR4, FcγR, Dectin, DC-SIGN, scavenger receptors)
2. Actin cytoskeleton dynamics during phagocytosis and its implications for phagocytic functions.
3. Molecular processes involved in phagosome formation and sealing in phagocytic cells of the immune system.
4. Vesicular trafficking.
5. Phagocytosis of bacterial, fungal and parasitic pathogens.
6. Phagocytosis and antigen presentation.
7. Phagocytosis of apoptotic cells and resolution of inflammation.
8. Phagocytosis of cancer cells in the context of anti-tumor immunity.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
