scholarly journals The Phagocytic Code Regulating Phagocytosis of Mammalian Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Tom O. J. Cockram ◽  
Jacob M. Dundee ◽  
Alma S. Popescu ◽  
Guy C. Brown
Keyword(s):  
Mammalian Cells ◽  
The Body ◽  
Psychiatric Disease ◽  
Target Cells ◽  
Immune Disease ◽  
Neuronal Synapses ◽  
Galectin 3 ◽  
A Cell ◽  
Infected Cells ◽  
Dying Cells

Mammalian phagocytes can phagocytose (i.e. eat) other mammalian cells in the body if they display certain signals, and this phagocytosis plays fundamental roles in development, cell turnover, tissue homeostasis and disease prevention. To phagocytose the correct cells, phagocytes must discriminate which cells to eat using a ‘phagocytic code’ - a set of over 50 known phagocytic signals determining whether a cell is eaten or not - comprising find-me signals, eat-me signals, don’t-eat-me signals and opsonins. Most opsonins require binding to eat-me signals – for example, the opsonins galectin-3, calreticulin and C1q bind asialoglycan eat-me signals on target cells - to induce phagocytosis. Some proteins act as ‘self-opsonins’, while others are ‘negative opsonins’ or ‘phagocyte suppressants’, inhibiting phagocytosis. We review known phagocytic signals here, both established and novel, and how they integrate to regulate phagocytosis of several mammalian targets - including excess cells in development, senescent and aged cells, infected cells, cancer cells, dead or dying cells, cell debris and neuronal synapses. Understanding the phagocytic code, and how it goes wrong, may enable novel therapies for multiple pathologies with too much or too little phagocytosis, such as: infectious disease, cancer, neurodegeneration, psychiatric disease, cardiovascular disease, ageing and auto-immune disease.

scholarly journals Galectin-3: Roles in Neurodevelopment, Neuroinflammation, and Behavior

Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 798
Author(s):  
Ivan Srejovic ◽  
Dragica Selakovic ◽  
Nemanja Jovicic ◽  
Vladimir Jakovljević ◽  
Miodrag L. Lukic ◽  
...  
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Mammalian Cells ◽  
Protective Role ◽  
Target Cells ◽  
Adult Mice ◽  
Pathological Conditions ◽  
Apoptotic Effect ◽  
Galectin 3 ◽  
The Central Nervous System

There is a plethora of evidence to suggest that Galectin-3 plays an important role in normal functions of mammalian cells, as well as in different pathogenic conditions. This review highlights recent data published by researchers, including our own team, on roles of Galectin-3 in the nervous system. Here, we discuss the roles of Galectin-3 in brain development, its roles in glial cells, as well as the interactions of glial cells with other neural and invading cells in pathological conditions. Galectin-3 plays an important role in the pathogenesis of neuroinflammatory and neurodegenerative disorders, such as multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. On the other hand, there is also evidence of the protective role of Galectin-3 due to its anti-apoptotic effect in target cells. Interestingly, genetic deletion of Galectin-3 affects behavioral patterns in maturing and adult mice. The results reviewed in this paper and recent development of highly specific inhibitors suggests that Galectin-3 may be an important therapeutic target in pathological conditions including the disorders of the central nervous system.

scholarly journals Analysis of General Humoral Immunity HIV Dynamics Model with HAART and Distributed Delays

Mathematics ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 157 ◽  
Author(s):  
A. Elaiw ◽  
E. Elnahary
Keyword(s):  
Hiv Infection ◽  
The Body ◽  
Target Cells ◽  
Nonlinear Functions ◽  
Dynamics Model ◽  
Therapeutic Modalities ◽  
Hiv Dynamics ◽  
Highly Active ◽  
Infected Cells ◽  
Theoretical Results

This paper deals with the study of an HIV dynamics model with two target cells, macrophages and CD4 + T cells and three categories of infected cells, short-lived, long-lived and latent in order to get better insights into HIV infection within the body. The model incorporates therapeutic modalities such as reverse transcriptase inhibitors (RTIs) and protease inhibitors (PIs). The model is incorporated with distributed time delays to characterize the time between an HIV contact of an uninfected target cell and the creation of mature HIV. The effect of antibody on HIV infection is analyzed. The production and removal rates of the ten compartments of the model are given by general nonlinear functions which satisfy reasonable conditions. Nonnegativity and ultimately boundedness of the solutions are proven. Using the Lyapunov method, the global stability of the equilibria of the model is proven. Numerical simulations of the system are provided to confirm the theoretical results. We have shown that the antibodies can play a significant role in controlling the HIV infection, but it cannot clear the HIV particles from the plasma. Moreover, we have demonstrated that the intracellular time delay plays a similar role as the Highly Active Antiretroviral Therapies (HAAT) drugs in eliminating the HIV particles.

Exosomes: the ideal nanovectors for biodelivery

2013 ◽  
Vol 394 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Stefano Fais ◽  
Mariantonia Logozzi ◽  
Luana Lugini ◽  
Cristina Federici ◽  
Tommaso Azzarito ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Pathological Condition ◽  
Biological Properties ◽  
The Body ◽  
Target Cells ◽  
Positive Effects ◽  
Gender And Age ◽  
Infected Cells ◽  
Properties Of Materials ◽  
Potential Use

Abstract Nanomedicine aims to exploit the improved and often novel physical, chemical, and biological properties of materials at the nanometric scale, possibly with the highest level of biomimetism, an approach that simulates what occurs in nature. Although extracellularly released vesicles include both microvesicles (MVs) and exosomes, only exosomes have the size that may be considered suitable for potential use in nanomedicine. In fact, recent reports have shown that exosomes are able to interact with target cells within an organ or at a distance using different mechanisms. Much is yet to be understood about exosomes, and currently, we are looking at the visible top of an iceberg, with most of what we have to understand on these nanovesicles still under the sea. In fact, we know that exosomes released by normal cells always trigger positive effects, whereas those released by cells in pathological condition, such as tumor or infected cells, may induce undesired, dangerous, and mostly unknown effects, but we cannot exclude the possibility that exosomes may also be detrimental for the body in normal conditions. However, whether we consider extracellular vesicles as a whole, thus including MVs, it appears that even in normal conditions, extracellular vesicles may lead to unwanted effects, depending on gender and age. This review aims to critically emphasize existing data in the literature that support the possible roles of exosomes in both diagnostic and therapeutic scopes.

scholarly journals The NS5A/NS5 Proteins of Viruses from Three Genera of the Family Flaviviridae Are Phosphorylated by Associated Serine/Threonine Kinases

1998 ◽  
Vol 72 (7) ◽  
pp. 6199-6206 ◽  
Author(s):  
Karen E. Reed ◽  
Alexander E. Gorbalenya ◽  
Charles M. Rice
Keyword(s):  
Mammalian Cells ◽  
Yellow Fever Virus ◽  
Diarrhea Virus ◽  
The Family ◽  
A Cell ◽  
Infected Cells ◽  
Threonine Kinases ◽  
The One ◽  
Viral Diarrhea Virus

ABSTRACT Phosphorylation of the expressed NS5A protein of hepatitis C virus (HCV), a member of the Hepacivirus genus of the familyFlaviviridae, has been demonstrated in mammalian cells and in a cell-free assay by an associated kinase activity. In this report, phosphorylation is also shown for the NS5A and NS5 proteins, respectively, of bovine viral diarrhea virus (BVDV) and yellow fever virus (YF), members of the other two established genera in this family. Phosphorylation of BVDV NS5A and YF NS5 was observed in infected cells, transient expression experiments, and a cell-free assay similar to the one developed for HCV NS5A. Phosphoamino acid analyses indicated that all three proteins were phosphorylated by serine/threonine kinases. Similarities in the properties of BVDV NS5A, YF NS5, and HCV NS5A phosphorylation in vitro further suggested that closely related kinases or the same kinase may phosphorylate these viral proteins. Conservation of this trait among three quite distantly related viruses representing three separate genera suggests that phosphorylation of the NS5A/NS5 proteins or their association with cellular kinases may play an important role in the flavivirus life cycle.

scholarly journals Microbial Phagocytic Receptors and Their Potential Involvement in Cytokine Induction in Macrophages

2021 ◽  
Vol 12 ◽  
Author(s):  
Yan Lin Fu ◽  
Rene E. Harrison
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Cytokine Production ◽  
Adaptive Immune Response ◽  
The Body ◽  
Target Cells ◽  
Surface Receptors ◽  
Internalization Process ◽  
Dying Cells

Phagocytosis is an essential process for the uptake of large (>0.5 µm) particulate matter including microbes and dying cells. Specialized cells in the body perform phagocytosis which is enabled by cell surface receptors that recognize and bind target cells. Professional phagocytes play a prominent role in innate immunity and include macrophages, neutrophils and dendritic cells. These cells display a repertoire of phagocytic receptors that engage the target cells directly, or indirectly via opsonins, to mediate binding and internalization of the target into a phagosome. Phagosome maturation then proceeds to cause destruction and recycling of the phagosome contents. Key subsequent events include antigen presentation and cytokine production to alert and recruit cells involved in the adaptive immune response. Bridging the innate and adaptive immunity, macrophages secrete a broad selection of inflammatory mediators to orchestrate the type and magnitude of an inflammatory response. This review will focus on cytokines produced by NF-κB signaling which is activated by extracellular ligands and serves a master regulator of the inflammatory response to microbes. Macrophages secrete pro-inflammatory cytokines including TNFα, IL1β, IL6, IL8 and IL12 which together increases vascular permeability and promotes recruitment of other immune cells. The major anti-inflammatory cytokines produced by macrophages include IL10 and TGFβ which act to suppress inflammatory gene expression in macrophages and other immune cells. Typically, macrophage cytokines are synthesized, trafficked intracellularly and released in response to activation of pattern recognition receptors (PRRs) or inflammasomes. Direct evidence linking the event of phagocytosis to cytokine production in macrophages is lacking. This review will focus on cytokine output after engagement of macrophage phagocytic receptors by particulate microbial targets. Microbial receptors include the PRRs: Toll-like receptors (TLRs), scavenger receptors (SRs), C-type lectin and the opsonic receptors. Our current understanding of how macrophage receptor stimulation impacts cytokine production is largely based on work utilizing soluble ligands that are destined for endocytosis. We will instead focus this review on research examining receptor ligation during uptake of particulate microbes and how this complex internalization process may influence inflammatory cytokine production in macrophages.

scholarly journals Visualizing the ribonucleoprotein content of single bunyavirus virions reveals more efficient genome packaging in the arthropod host

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Erick Bermúdez-Méndez ◽  
Eugene A. Katrukha ◽  
Cindy M. Spruit ◽  
Jeroen Kortekaas ◽  
Paul J. Wichgers Schreur
Keyword(s):  
Single Molecule ◽  
Mammalian Cells ◽  
Rift Valley Fever Virus ◽  
Progeny Virus ◽  
Genome Packaging ◽  
Valley Fever ◽  
A Genome ◽  
A Cell ◽  
Infected Cells

AbstractBunyaviruses have a genome that is divided over multiple segments. Genome segmentation complicates the generation of progeny virus, since each newly formed virus particle should preferably contain a full set of genome segments in order to disseminate efficiently within and between hosts. Here, we combine immunofluorescence and fluorescence in situ hybridization techniques to simultaneously visualize bunyavirus progeny virions and their genomic content at single-molecule resolution in the context of singly infected cells. Using Rift Valley fever virus and Schmallenberg virus as prototype tri-segmented bunyaviruses, we show that bunyavirus genome packaging is influenced by the intracellular viral genome content of individual cells, which results in greatly variable packaging efficiencies within a cell population. We further show that bunyavirus genome packaging is more efficient in insect cells compared to mammalian cells and provide new insights on the possibility that incomplete particles may contribute to bunyavirus spread as well.

scholarly journals Visualizing the RNP content of single bunyavirus virions reveals more efficient genome packaging in the arthropod host

2020 ◽  
Author(s):  
Erick Bermúdez-Méndez ◽  
Eugene Katrukha ◽  
Cindy Spruit ◽  
Jeroen Kortekaas ◽  
Paul Wichgers Schreur
Keyword(s):  
Single Molecule ◽  
Mammalian Cells ◽  
Rift Valley Fever Virus ◽  
Progeny Virus ◽  
Genome Packaging ◽  
Valley Fever ◽  
A Genome ◽  
A Cell ◽  
Infected Cells

Abstract Bunyaviruses have a genome that is divided over multiple segments. Genome segmentation complicates the generation of progeny virus, since each newly formed virus particle should preferably contain a full set of genome segments in order to disseminate efficiently within and between hosts. Here, we combine immunofluorescence and fluorescence in situ hybridization techniques to simultaneously visualize bunyavirus progeny virions and their genomic content at single-molecule resolution in the context of singly infected cells. Using Rift Valley fever virus and Schmallenberg virus as prototype tri-segmented bunyaviruses, we show that bunyavirus genome packaging is influenced by the intracellular viral genome content of individual cells, which results in greatly variable packaging efficiencies within a cell population. We further show that bunyavirus genome packaging is more efficient in insect cells compared to mammalian cells and provide new insights on the possibility that incomplete particles may contribute to bunyavirus spread as well.

scholarly journals Effect of Natural Compounds on NK Cell Activation

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Malgorzata Grudzien ◽  
Andrzej Rapak
Keyword(s):  
Nk Cells ◽  
Cell Activation ◽  
Nk Cell ◽  
Death Receptor ◽  
Adaptive Immune Response ◽  
The Body ◽  
Target Cells ◽  
Surface Receptors ◽  
Microbial Infections ◽  
A Cell

Natural killer (NK) cells are lymphocytes of the innate immune system that survey the body for stressed and abnormal cells. The integration of signals that they receive through various inhibitory and activating cell surface receptors controls their activation and ability to kill target cells and produce cytokines. In this manner, phenotypically and functionally distinct subsets of NK cells help protect against microbial infections and cancer and shape the adaptive immune response. NK cells can use two different mechanisms to kill their targets, either by cytotoxic granule exocytosis or by induction of death receptor-mediated apoptosis. Death ligands belong to the tumor necrosis factor (TNF) family of ligands. Upon release in close proximity to a cell slated for killing, perforin forms pores in the cell membrane of the target cell through which granzymes and associated molecules can enter and induce apoptosis. NK cells are also involved in antibody-dependent cellular toxicity via the CD16 receptor. In addition to target recognition, NK cells can be also activated by treatment with multiple compounds with stimulatory properties. Apart from interleukins, which belong to the best characterized group of NK cell-stimulating compounds, vitamins and constituents extracted from plants also display the ability to activate NK cells. The current review characterizes several groups of NK cell-activating compounds: vitamins belonging to classes A, B, C, D, and E, polysaccharides, lectins, and a number of phytochemicals used in cancer research, exhibiting stimulatory properties when applied to NK cells. Although in most cases the exact mechanism of action is not known, constituents described in this review seem to be promising candidates for NK cell-stimulating drugs.

scholarly journals BACTENECINS AS CELL-PENETRATING PEPTIDES

2019 ◽  
Vol 19 (1S) ◽  
pp. 178-179
Author(s):  
O V Shamova ◽  
A S Nazarov ◽  
P M Kopeykin ◽  
I V Kudryavtsev ◽  
N A Grudinina ◽  
...  
Keyword(s):  
Mammalian Cells ◽  
Cell Penetrating Peptides ◽  
Eukaryotic Cells ◽  
Target Cells ◽  
Medium Temperature ◽  
Cell Penetrating ◽  
Internalization Process ◽  
Infected Cells ◽  
Truncated Variants

Cell-Penetrating Peptides (CPPs) are molecules that can easily internalize into eukaryotic cells, as well as deliver across their membranes a variety of compounds (proteins, nucleic acids, liposomes, nanoparticles, etc.). CPPs are considered as promising components of anticancer drugs, serving for delivery of active ingredients into malignant cells, therefore, a detailed study of a mechanism of action of CPPs and search for novel, more effective peptides are vital tasks of current biological and medical research. An ability of proline-rich peptides bactenecins (ChBac5, ChBac3.4, mini-ChBac7.5Na) and their truncated variants to penetrate into eukaryotic cells has been explored. By means of flow cytometry and confocal microscopy, we found that these peptides, tagged with a fluorescent dye BODIPY FL, rapidly penetrated into tumor cells and, to a lesser extent, into normal mammalian cells in vitro. The dependence of the internalization process on the medium temperature and energy metabolism of target cells was studied. The obtained data on the cell-penetratin activity of caprine bactenecins confirm the prospect of further investigations of these peptides as prototypes of new compounds - carriers of drugs into malignant or infected cells.

The effects of Cyclosporin-A (CYA) on the Ultrastructure of Gingival Mast Cells (GMC) in Behcet's disease (BD)

1990 ◽  
Vol 48 (3) ◽  
pp. 358-359
Author(s):  
Oktay Arda ◽  
Ulkü Noyan ◽  
Selgçk Yilmaz ◽  
Mustafa Taşyürekli ◽  
İsmail Seçkin ◽  
...  
Keyword(s):  
Unknown Etiology ◽  
Control Group ◽  
Target Cells ◽  
Gingival Hyperplasia ◽  
Cellular Activity ◽  
Direct Relation ◽  
Immune Disease ◽  
Genital Ulceration ◽  
Functional Changes ◽  
The Third

Turkish dermatologist, H. Beheet described the disease as recurrent triad of iritis, oral aphthous lesions and genital ulceration. Auto immune disease is the recent focus on the unknown etiology which is still being discussed. Among the other immunosupressive drugs, CyA included in it's treatment newly. One of the important side effects of this drug is gingival hyperplasia which has a direct relation with the presence of teeth and periodontal tissue. We are interested in the ultrastructure of immunocompetent target cells that were affected by CyA in BD.Three groups arranged in each having 5 patients with BD. Control group was the first and didn’t have CyA treatment. Patients who had CyA, but didn’t show gingival hyperplasia assembled the second group. The ones displaying gingival hyperplasia following CyA therapy formed the third group. GMC of control group and their granules are shown in FIG. 1,2,3. GMC of the second group presented initiation of supplementary cellular activity and possible maturing functional changes with the signs of increased number of mitochondria and accumulation of numerous dense cored granules next to few normal ones, FIG. 4,5,6.

Sign in / Sign up

Export Citation Format

Share Document