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Frontiers in Immunology 2023
Topics: Gene Expression Regulation; Macrophages
PubMed: 38022640
DOI: 10.3389/fimmu.2023.1321064 -
Fish & Shellfish Immunology Jan 2024In the present study, we review the structure and function of fish spleen with special emphasis on its condition in Elasmobranchs, Teleosts and Lungfish. Apart from the... (Review)
Review
In the present study, we review the structure and function of fish spleen with special emphasis on its condition in Elasmobranchs, Teleosts and Lungfish. Apart from the amount of splenic lymphoid tissue, the histological organization of the organ ensures the existence of areas involved in antigen trapping, the ellipsoids, and exhibit numerous melano-macrophages which appear isolated or forming the so-called melano-macrophage centres. An extensive discussion on the functional significance of these centres conclude that they are mere accumulations of macrophages consequence of tissue homeostasis rather than primitive germinal centres, as proposed by some authors.
Topics: Animals; Spleen; Lymphoid Tissue; Macrophages; Fishes
PubMed: 38086514
DOI: 10.1016/j.fsi.2023.109280 -
Medicina (Kaunas, Lithuania) Nov 2023Idiopathic pulmonary fibrosis (IPF) is a devastating disease of unknown etiology with limited treatment options. The role of the immune system in IPF has received... (Review)
Review
Idiopathic pulmonary fibrosis (IPF) is a devastating disease of unknown etiology with limited treatment options. The role of the immune system in IPF has received increasing attention. Uncontrolled immune responses drive the onset and progression of IPF. This article provides an overview of the role of innate immune cells (including macrophages, neutrophils, mast cells, eosinophils, dendritic cells, nature killer cells, nature kill cells and γδ T cells) and adaptive immune cells (including Th1 cells, Th2 cells, Th9 cells, Th17 cells, Th22 cells, cytotoxic T cells, B lymphocytes and Treg cells) in IPF. In addition, we review the current status of pharmacological treatments for IPF and new developments in immunotherapy. A deeper comprehension of the immune system's function in IPF may contribute to the development of targeted immunomodulatory therapies that can alter the course of the disease.
Topics: Humans; Idiopathic Pulmonary Fibrosis; T-Lymphocytes, Regulatory; Macrophages; Neutrophils; Mast Cells
PubMed: 38004032
DOI: 10.3390/medicina59111984 -
Apoptosis : An International Journal on... Dec 2023Pulmonary fibrosis (PF) is a disease in which excessive extracellular matrix (ECM) accumulation occurs in pulmonary mesenchyme, which induces the destruction of alveolar... (Review)
Review
Pulmonary fibrosis (PF) is a disease in which excessive extracellular matrix (ECM) accumulation occurs in pulmonary mesenchyme, which induces the destruction of alveolar structures and poor prognosis. Macrophage death is responsible for ECM accumulation after alveolar epithelial injury in PF. Depending on the local micro-environments, macrophages can be polarized to either classically activated (M1) or alternatively activated (M2) macrophage phenotypes. In general, M1 macrophages can promote inflammation and sterilization, stop the continuous damage process and prevent excessive repair, while M2 macrophages are anti-inflammatory and promote tissue repair, and excessive M2 macrophage activity may inhibit the absorption and degradation of ECM. Emerging evidence has revealed that death forms such as pyroptosis mediated by inflammasome affect polarization direction and ultimately lead to the development of PF. Pharmacological manipulation of macrophages death signals may serve as a logical therapeutic strategy for PF. This review will focus on the current state of knowledge regarding the regulation and underlying mechanisms of macrophages and their mediators in the influence of macrophage death on the development of PF. We expect to provide help in developing effective therapeutic strategies in clinical settings.
Topics: Humans; Macrophages, Alveolar; Pulmonary Fibrosis; Apoptosis; Macrophages; Inflammation
PubMed: 37707713
DOI: 10.1007/s10495-023-01888-4 -
Frontiers in Immunology 2023Nonalcoholic fatty liver disease (NAFLD) is an expanding worldwide health concern, and the underlying mechanisms contributing to its progression still need further... (Review)
Review
Nonalcoholic fatty liver disease (NAFLD) is an expanding worldwide health concern, and the underlying mechanisms contributing to its progression still need further exploration. Neutrophil extracellular traps (NETs) are intricate formations comprised of nuclear constituents and diverse antimicrobial granules that are released into the extracellular milieu by activated neutrophils upon various triggers, which play a pivotal part in the onset and advancement of NAFLD. NETs actively participate in the genesis of NAFLD by fostering oxidative stress and inflammation, ultimately resulting in hepatic fat accumulation and the escalation of liver injury. Recent insights into the interaction with other hepatic immune populations and mediators, such as macrophages and T regulatory cells, have revealed several important mechanisms that can trigger further liver injury. In conclusion, the formation of NETs emerged as an important factor in the development of NAFLD, offering a promising target for innovative therapeutic approaches against this debilitating condition. This comprehensive review seeks to compile existing studies exploring the involvement of NETs in the genesis of NAFLD and their influence on the immune response throughout the progression of NAFLD.
Topics: Humans; Non-alcoholic Fatty Liver Disease; Extracellular Traps; Inflammation; Neutrophils
PubMed: 38022519
DOI: 10.3389/fimmu.2023.1292679 -
Frontiers in Immunology 2023Despite tremendous efforts to exploit effective therapeutic strategies, most glioblastoma (GBM) inevitably relapse and become resistant to therapies, including... (Review)
Review
Despite tremendous efforts to exploit effective therapeutic strategies, most glioblastoma (GBM) inevitably relapse and become resistant to therapies, including radiotherapy and immunotherapy. The tumor microenvironment (TME) of recurrent GBM (rGBM) is highly immunosuppressive, dominated by tumor-associated macrophages (TAMs). TAMs consist of tissue-resident microglia and monocyte-derived macrophages (MDMs), which are essential for favoring tumor growth, invasion, angiogenesis, immune suppression, and therapeutic resistance; however, restricted by the absence of potent methods, the heterogeneity and plasticity of TAMs in rGBM remain incompletely investigated. Recent application of single-cell technologies, such as single-cell RNA-sequencing has enabled us to decipher the unforeseen diversity and dynamics of TAMs and to identify new subsets of TAMs which regulate anti-tumor immunity. Here, we first review hallmarks of the TME, progress and challenges of immunotherapy, and the biology of TAMs in the context of rGBM, including their origins, categories, and functions. Next, from a single-cell perspective, we highlight recent findings regarding the distinctions between tissue-resident microglia and MDMs, the identification and characterization of specific TAM subsets, and the dynamic alterations of TAMs during tumor progression and treatment. Last, we briefly discuss the potential of TAM-targeted strategies for combination immunotherapy in rGBM. We anticipate the comprehensive understanding of the diversity and dynamics of TAMs in rGBM will shed light on further improvement of immunotherapeutic efficacy in rGBM.
Topics: Humans; Tumor-Associated Macrophages; Glioblastoma; Macrophages; Chronic Disease; Recurrence; Tumor Microenvironment
PubMed: 37731483
DOI: 10.3389/fimmu.2023.1238233 -
Aging Cell Dec 2023Advancements in longevity research have provided insights into the impact of cardiac aging on the structural and functional aspects of the heart. Notable changes include... (Review)
Review
Advancements in longevity research have provided insights into the impact of cardiac aging on the structural and functional aspects of the heart. Notable changes include the gradual remodeling of the myocardium, the occurrence of left ventricular hypertrophy, and the decline in both systolic and diastolic functions. Macrophages, a type of immune cell, play a pivotal role in innate immunity by serving as vigilant agents against pathogens, facilitating wound healing, and orchestrating the development of targeted acquired immune responses. Distinct subsets of macrophages are present within the cardiac tissue and demonstrate varied functions in response to myocardial injury. The differentiation of cardiac macrophages according to their developmental origin has proven to be a valuable strategy in identifying reparative macrophage populations, which originate from embryonic cells and reside within the tissue, as well as inflammatory macrophages, which are derived from monocytes and recruited to the heart. These subsets of macrophages possess unique characteristics and perform distinct functions. This review aims to summarize the current understanding of the roles and phenotypes of cardiac macrophages in various conditions, including the steady state, aging, and other pathological conditions. Additionally, it will highlight areas that require further investigation to expand our knowledge in this field.
Topics: Heart; Macrophages; Myocardium; Monocytes
PubMed: 37817547
DOI: 10.1111/acel.14008 -
Immunological Reviews Oct 2023The clearance of dead and dying cells, termed efferocytosis, is a rapid and efficient process and one that is critical for organismal health. The extraordinary speed and... (Review)
Review
The clearance of dead and dying cells, termed efferocytosis, is a rapid and efficient process and one that is critical for organismal health. The extraordinary speed and efficiency with which dead cells are detected and engulfed by immune cells within tissues presents a challenge to researchers who wish to unravel this fascinating process, since these fleeting moments of uptake are almost impossible to catch in vivo. In recent years, the fruit fly (Drosophila melanogaster) embryo has emerged as a powerful model to circumvent this problem. With its abundance of dying cells, specialist phagocytes and relative ease of live imaging, the humble fly embryo provides a unique opportunity to catch and study the moment of cell engulfment in real-time within a living animal. In this review, we explore the recent advances that have come from studies in the fly, and how live imaging and genetics have revealed a previously unappreciated level of diversity in the efferocytic program. A variety of efferocytic strategies across the phagocytic cell population ensure efficient and rapid clearance of corpses wherever death is encountered within the varied and complex setting of a multicellular living organism.
Topics: Animals; Humans; Drosophila melanogaster; Apoptosis; Phagocytosis; Phagocytes; Drosophila
PubMed: 37589239
DOI: 10.1111/imr.13266 -
Frontiers in Immunology 2023Cell death is an important aspect of atherosclerotic plaque development. Insufficient efferocytosis of death cells by phagocytic macrophages leads to the buildup of a... (Review)
Review
Cell death is an important aspect of atherosclerotic plaque development. Insufficient efferocytosis of death cells by phagocytic macrophages leads to the buildup of a necrotic core that impacts stability of the plaque. Furthermore, in the presence of calcium and phosphate, apoptotic bodies resulting from death cells can act as nucleation sites for the formation of calcium phosphate crystals, mostly in the form of hydroxyapatite, which leads to calcification of the atherosclerotic plaque, further impacting plaque stability. Excessive uptake of cholesterol-loaded oxidized LDL particles by macrophages present in atherosclerotic plaques leads to foam cell formation, which not only reduces their efferocytosis capacity, but also can induce apoptosis in these cells. The resulting apoptotic bodies can contribute to calcification of the atherosclerotic plaque. Moreover, other forms of macrophage cell death, such as pyroptosis, necroptosis, parthanatos, and ferroptosis can also contribute by similar mechanisms to plaque calcification. This review focuses on macrophage death in atherosclerosis, and its potential role in calcification. Reducing macrophage cell death and/or increasing their efferocytosis capacity could be a novel therapeutic strategy to reduce the formation of a necrotic core and calcification and thereby improving atherosclerotic plaque stability.
Topics: Humans; Plaque, Atherosclerotic; Atherosclerosis; Macrophages; Apoptosis; Necrosis; Calcinosis
PubMed: 37469518
DOI: 10.3389/fimmu.2023.1215612 -
Frontiers in Immunology 2023Atherosclerosis is a complex inflammatory disease that affects the arteries and can lead to severe complications such as heart attack and stroke. Macrophages, a type of... (Review)
Review
Atherosclerosis is a complex inflammatory disease that affects the arteries and can lead to severe complications such as heart attack and stroke. Macrophages, a type of immune cell, play a crucial role in atherosclerosis initiation and progression. Emerging studies revealed that ion channels regulate macrophage activation, polarization, phagocytosis, and cytokine secretion. Moreover, macrophage ion channel dysfunction is implicated in macrophage-derived foam cell formation and atherogenesis. In this context, exploring the regulatory role of ion channels in macrophage function and their impacts on the progression of atherosclerosis emerges as a promising avenue for research. Studies in the field will provide insights into novel therapeutic targets for the treatment of atherosclerosis.
Topics: Humans; Atherosclerosis; Macrophages; Foam Cells; Myocardial Infarction; Phagocytosis
PubMed: 37588590
DOI: 10.3389/fimmu.2023.1225178