1.Reactive oxygen intermediate production of phagocytes from human cord blood.
Hae Jeong KIM ; Noh Heui MYEONG ; Bok Soo LEE ; Chang Duk JUN ; Hun Taeg CHUNG
Korean Journal of Immunology 1992;14(1):97-105
No abstract available.
Fetal Blood*
;
Humans*
;
Oxygen*
;
Phagocytes*
2.Neutrophils in Immunity.
Journal of Bacteriology and Virology 2012;42(2):172-176
Neutrophils are the most abundant white blood cells in the peripheral blood and have long been recognized as the major phagocytes in acute infection by destroying extracellular pathogens. Although research on neutrophils hampered by intractability in the experiments, the newly discovered effector functions of neutrophils includes granular proteins, and cytokines, extracellular traps. With all effector mechanism neutrophils play a critical role in the pathogenesis of acute and chronic infection, autoimmunity and cancer.
Autoimmunity
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Cytokines
;
Inflammation
;
Leukocytes
;
Neutrophils
;
Phagocytes
;
Proteins
3.Engulfment signals and the phagocytic machinery for apoptotic cell clearance.
Experimental & Molecular Medicine 2017;49(5):e331-
The clearance of apoptotic cells is an essential process for tissue homeostasis. To this end, cells undergoing apoptosis must display engulfment signals, such as ‘find-me' and ‘eat-me' signals. Engulfment signals are recognized by multiple types of phagocytic machinery in phagocytes, leading to prompt clearance of apoptotic cells. In addition, apoptotic cells and phagocytes release tolerogenic signals to reduce immune responses against apoptotic cell-derived self-antigens. Here we discuss recent advances in our knowledge of engulfment signals, the phagocytic machinery and the signal transduction pathways for apoptotic cell engulfment.
Apoptosis
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Autoantigens
;
Homeostasis
;
Phagocytes
;
Signal Transduction
4.Fever.
Korean Journal of Pediatrics 2007;50(2):121-126
Fever has been recognized as a cardinal feature of disease since antiquity, but only recently has the pathophysiology of fever come to be understood. It became clear that the ultimate cause of fever is not a bacterial product (a so-called exogenous pyrogen) but a product of host inflammatory cells (i.e., an endogenous pyrogen). Many studies have demonstrated that mononuclear phagocytes are the principal source of endogenous pyrogen and that a variety of mononuclear cell products can mediate the febrile response. Cytokines are also important as mediators of the acute-phase response to infection and inflammation.
Acute-Phase Reaction
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Cytokines
;
Fever*
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Inflammation
;
Phagocytes
5.Autophagy in neutrophils
Sanjeeb SHRESTHA ; Jae Man LEE ; Chang Won HONG
The Korean Journal of Physiology and Pharmacology 2020;24(1):1-10
Autophagy is a highly conserved intracellular degradation and energy-recycling mechanism that contributes to the maintenance of cellular homeostasis. Extensive researches over the past decades have defined the role of autophagy innate immune cells. In this review, we describe the current state of knowledge regarding the role of autophagy in neutrophil biology and a picture of molecular mechanism underlying autophagy in neutrophils. Neutrophils are professional phagocytes that comprise the first line of defense against pathogen. Autophagy machineries are highly conserved in neutrophils. Autophagy is not only involved in generalized function of neutrophils such as differentiation in bone marrow but also plays crucial role effector functions of neutrophils such as granule formation, degranulation, neutrophil extracellular traps release, cytokine production, bactericidal activity and controlling inflammation. This review outlines the current understanding of autophagy in neutrophils and provides insight towards identification of novel therapeutics targeting autophagy in neutrophils.
Autophagy
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Biology
;
Bone Marrow
;
Extracellular Traps
;
Homeostasis
;
Inflammation
;
Neutrophils
;
Phagocytes
6.Extracellular Vesicles of Neutrophils.
Immune Network 2018;18(6):e43-
Extracellular vesicles (EVs) are membrane-derived vesicles that mediate intercellular communications. As professional phagocytes, neutrophils also produce EVs in response to various inflammatory stimuli during inflammatory processes. Neutrophil-derived EVs can be categorized into 2 subtypes according to the mechanism of generation. Neutrophil-derived trails (NDTRs) are generated from migrating neutrophils. The uropods of neutrophils are elongated by adhesion to endothelial cells, and small parts of the uropods are detached, leaving submicrometer-sized NDTRs. Neutrophil-derived microvesicles (NDMVs) are generated from neutrophils which arrived at the inflammatory foci. Membrane blebbing occurs in response to various stimuli at the inflammatory foci, and small parts of the blebs are detached from the neutrophils, leaving NDMVs. These 2 subtypes of neutrophil-derived EVs share common features such as membrane components, receptors, and ligands. However, there are substantial differences between these 2 neutrophil-derived EVs. NDTRs exert pro-inflammatory functions by guiding subsequent immune cells through the inflammatory foci. On the other hand, NDMVs exert anti-inflammatory functions by limiting the excessive immune responses of nearby cells. This review outlines the current understanding of the different subtypes of neutrophil-derived EVs and provides insights into the clinical relevance of neutrophil-derived EVs.
Blister
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Endothelial Cells
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Extracellular Vesicles*
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Hand
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Ligands
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Membranes
;
Neutrophils*
;
Phagocytes
7.Tactics of Mycobacterium avium subsp. paratuberculosis for intracellular survival in mononuclear phagocytes.
Seng Ryong WOO ; Charles J CZUPRYNSKI
Journal of Veterinary Science 2008;9(1):1-8
Johne's disease is a condition that refers to chronic granulomatous enteritis in ruminants. It is believed that survival and replication of Mycobacterium (M.) paratuberculosis in mononuclear phagocytes plays an important role in the pathogenesis of Johne's disease. However, it is not clear how M. paratuberculosis survives for long time periods in mononuclear phagocytes, nor is it clear which factors trigger multiplication of these bacilli and result in the development of Johne's disease. Investigating the intracellular fate of M. paratuberculosis is challenging because of its very slow growth (more than two months to form visible colonies on media). Existing animal models also have limitations. Despite those obstacles, there has been progress in understanding the intracellular survival tactics of M. paratuberculosis and the host response against them. In this review, we compare known aspects of the intracellular survival tactics of M. paratuberculosis with those of other mycobacterial species, and consider possible mycobactericidal mechanisms of mononuclear phagocytes.
Animals
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Leukocytes, Mononuclear/*microbiology
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Mycobacterium avium subsp. paratuberculosis/*physiology
;
Phagocytes/*microbiology
8.Morphologic and Immunohistochemical Studies of Attached Retina in Intravitreal Silicone Oil.
In Taek KIM ; Sang Min PARK ; Bo Young JUN
Journal of the Korean Ophthalmological Society 2001;42(2):396-400
Intraocular silicone oil is known to induce irreversible histological changes in retina. We enucleated an eyeball which was filled with silicone oil for 6 years following pars plana vitrectomy for the treatment of proliferative vitreoretinopathy. Purified 1000 cs silicone oil was used. The reattached retina tissue was examined histopathologically and immunohistochemically. Microscopic examination revealed severe retinal degenerations with many vaculoes in inner retina, the proliferation of glial cells, and the presence of phagocytes. The proliferation of the retinal pigment epithelium and the localized calcification of retinal tissues were also observed. Immunohistochemical study showed retinal tissue expressions of vimentin, S-100, and glial fibrillary acidic protein(GFAP). Electron microscopic examination of the retinal tissues demonstrated some phagocytes with large vacules, which probably had been filled with silicone oil. Our study confirmed that intravitreal silicone oil might damage the retinal tissues.
Neuroglia
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Phagocytes
;
Retina*
;
Retinal Degeneration
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Retinal Pigment Epithelium
;
Retinaldehyde
;
Silicone Oils*
;
Vimentin
;
Vitrectomy
;
Vitreoretinopathy, Proliferative
9.Recent advance in primary immune deficiency disorders.
Hyoung Jin KANG ; Hee Young SHIN ; Hyo Seop AHN
Korean Journal of Pediatrics 2009;52(6):649-654
The immune system is comprised of cells and molecules whose collective and coordinated response to the introduction of foreign substance is referred to as the immune response. Defense against microbes is mediated by the early reaction (innate immunity) and the late response (adaptive immunity). Innate immunity consists of the epithelial barrier, phagocytes, complement and natural killer cells. Adaptive immunity, a more complex defense reaction, consists of activation of later-developed lymphocytes that, when stimulated by exposure to infectious agents, increase in magnitude and defensive capabilities with each successive exposure. In this review we discuss recent advances in important primary immune deficiency disorders of innate immunity (chronic granulomatous disease, leukocyte adhesion deficiency) and adaptive immunity (severe combined immune deficiency, Wiskott-Aldrich syndrome).
Adaptive Immunity
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Complement System Proteins
;
Immune System
;
Immunity, Innate
;
Killer Cells, Natural
;
Leukocytes
;
Lymphocytes
;
Phagocytes
10.Genetic Polymorphism in Proteins of the Complement System.
Hyori KIM ; Dobeen HWANG ; Jungwon HAN ; Hwa Kyoung LEE ; Won Jun YANG ; Junyeong JIN ; Ki Hyun KIM ; Sang Il KIM ; Duck Kyun YOO ; Soohyun KIM ; Junho CHUNG
The Journal of the Korean Society for Transplantation 2016;30(2):59-68
The complement system is a part of the innate immune system that potentiates the ability of antibodies and phagocytic cells to clear microbes and damaged cells. The complement system consists of a number of proteins circulating as inactive precursors. It is stimulated mainly by three pathways: the classical pathway, the alternative pathway, and the lectin pathway. There are many genetic polymorphisms in this system, which can over-activate the immune system. In this study, we collected the polymorphisms reported to over-activate complement cascades that affect the immune system and induce autoimmune diseases.
Antibodies
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Autoimmune Diseases
;
Complement System Proteins*
;
Immune System
;
Phagocytes
;
Polymorphism, Genetic*