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Frontiers in Immunology 2019Quorum sensing is a type of cellular communication that was first described in bacteria, consisting of gene expression regulation in response to changes in... (Review)
Review
Quorum sensing is a type of cellular communication that was first described in bacteria, consisting of gene expression regulation in response to changes in cell-population density. Bacteria synthesize and secrete diffusive molecules called autoinducers, which concentration varies accordingly with cell density and can be detected by the producing cells themselves. Once autoinducer concentration reaches a critical threshold, all bacteria within the autoinducer-rich environment react by modifying their genetic expression and adopt a coordinated behavior (e.g., biofilm formation, virulence factor expression, or swarming motility). Recent advances highlight the possibility that such type of communication is not restricted to bacteria, but can exist among other cell types, including immune cells and more specifically monocyte-derived cells (1). For such cells, quorum sensing mechanisms may not only regulate their population size and synchronize their behavior at homeostasis but also alter their activity and function in unexpected ways during immune reactions. Although the nature of immune autoinducers and cellular mechanisms remains to be fully characterized, quorum sensing mechanisms in the immune system challenge our traditional conception of immune cell interactions and likely represent an important mode of communication at homeostasis or during an immune response. In this mini-review, we briefly present the prototypic features of quorum sensing in bacteria and discuss the existing evidence for quorum sensing within the immune system. Mainly, we review quorum sensing mechanisms among monocyte-derived cells, such as the regulation of inflammation by the density of monocyte-derived cells that produce nitric oxide and discuss the relevance of such models in the context of immune-related pathologies.
Topics: Animals; Cell Communication; Humans; Monocytes
PubMed: 31572366
DOI: 10.3389/fimmu.2019.02140 -
Seminars in Immunopathology Aug 2021Liver disorders due to infections are a substantial health concern in underdeveloped and industrialized countries. This includes not only hepatotropic viruses (e.g.,... (Review)
Review
Liver disorders due to infections are a substantial health concern in underdeveloped and industrialized countries. This includes not only hepatotropic viruses (e.g., hepatitis B, hepatitis C) but also bacterial and parasitic infections such as amebiasis, leishmaniasis, schistosomiasis, or echinococcosis. Recent studies of the immune mechanisms underlying liver disease show that monocytes play an essential role in determining patient outcomes. Monocytes are derived from the mononuclear phagocyte lineage in the bone marrow and are present in nearly all tissues of the body; these cells function as part of the early innate immune response that reacts to challenge by external pathogens. Due to their special ability to develop into tissue macrophages and dendritic cells and to change from an inflammatory to an anti-inflammatory phenotype, monocytes play a pivotal role in infectious and non-infectious liver diseases: they can maintain inflammation and support resolution of inflammation. Therefore, tight regulation of monocyte recruitment and termination of monocyte-driven immune responses in the liver is prerequisite to appropriate healing of organ damage. In this review, we discuss monocyte-dependent immune mechanisms underlying hepatic infectious disorders. Better understanding of these immune mechanisms may lead to development of new interventions to treat acute liver disease and prevent progression to organ failure.
Topics: Humans; Immunity, Innate; Liver Diseases; Macrophages; Monocytes
PubMed: 33829283
DOI: 10.1007/s00281-021-00852-1 -
Current Opinion in Hematology May 2020The well recognized plasticity and diversity, typical of monocytes and macrophages have recently been expanded by the knowledge that additional macrophage lineages... (Review)
Review
PURPOSE OF REVIEW
The well recognized plasticity and diversity, typical of monocytes and macrophages have recently been expanded by the knowledge that additional macrophage lineages originated directly from embryonic progenitors, populate and establish residency in all tissues examined so far. This review aims to summarize our current understanding on the diversity of monocyte/macrophage subtypes associated with the vasculature, their specific origins, and nature of their cross-talk with the endothelium.
RECENT FINDINGS
Taking stock of the many interactions between the endothelium and monocytes/macrophages reveals a far more intricate and ever-growing depth. In addition to circulating and surveilling the endothelium, monocytes can specifically be differentiated into patrolling cells that crawl on the surface of the endothelium and promote homeostasis. The conversion of classical to patrolling is endothelium-dependent uncovering an important functional link. In addition to patrolling cells, the endothelium also recruits and harbor an intimal-resident myeloid population that resides in the tunica intima in the absence of pathological insults. Moreover, the adventitia is populated with resident macrophages that support blood vessel integrity and prevent fibrosis.
SUMMARY
The last few years have witnessed a significant expansion in our knowledge of the many subtypes of monocytes and macrophages and their corresponding functional interactions with the vascular wall. In addition to surveying the endothelium for opportunities of diapedeses, monocyte and macrophages take residence in both the intima (as patrolling or resident) and in the adventitia. Their contributions to vascular function are broad and critical to homeostasis, regeneration, and expansion.
Topics: Animals; Cell Communication; Endothelial Cells; Endothelium, Vascular; Humans; Macrophages; Monocytes
PubMed: 32167947
DOI: 10.1097/MOH.0000000000000573 -
Frontiers in Immunology 2019Cancer immunotherapy relies on either restoring or activating the function of adaptive immune cells, mainly CD8 T lymphocytes. Despite impressive clinical success,... (Review)
Review
Cancer immunotherapy relies on either restoring or activating the function of adaptive immune cells, mainly CD8 T lymphocytes. Despite impressive clinical success, cancer immunotherapy remains ineffective in many patients due to the establishment of tumor resistance, largely dependent on the nature of tumor microenvironment. There are several cellular and molecular mechanisms at play, and the goal is to identify those that are clinically significant. Among the hematopoietic-derived cells, monocytes are endowed with high plasticity, responsible for their pro- and anti-tumoral function. Indeed, monocytes are involved in several cancer-associated processes such as immune-tolerance, metastatic spread, neoangiogenesis, and chemotherapy resistance; on the other hand, by presenting cancer-associated antigens, they can also promote and sustain anti-tumoral T cell response. Recently, by high throughput technologies, new findings have revealed previously underappreciated, profound transcriptional, epigenetic, and metabolic differences among monocyte subsets, which complement and expand our knowledge on the monocyte ontogeny, recruitment during steady state, and emergency hematopoiesis, as seen in cancer. The subdivision into discrete monocytes subsets, both in mice and humans, appears an oversimplification, whereas continuum subsets development is best for depicting the real condition. In this review, we examine the evidences sustaining the existence of a monocyte heterogeneity along with functional activities, at the primary tumor and at the metastatic niche. In particular, we describe how tumor-derived soluble factors and cell-cell contact reprogram monocyte function. Finally, we point out the role of monocytes in preparing and shaping the metastatic niche and describe relevant targetable molecules altering monocyte activities. We think that exploiting monocyte complexity can help identifying key pathways important for the treatment of cancer and several conditions where these cells are involved.
Topics: Animals; CCAAT-Enhancer-Binding Protein-alpha; Cell Plasticity; Humans; Immunotherapy; Monocytes; Myeloid-Derived Suppressor Cells; Neoplasms
PubMed: 31447834
DOI: 10.3389/fimmu.2019.01786 -
Cell Reports May 2023Monocytes are abundant immune cells that infiltrate inflamed organs. However, the majority of monocyte studies focus on circulating cells, rather than those in tissue....
Monocytes are abundant immune cells that infiltrate inflamed organs. However, the majority of monocyte studies focus on circulating cells, rather than those in tissue. Here, we identify and characterize an intravascular synovial monocyte population resembling circulating non-classical monocytes and an extravascular tissue-resident monocyte-lineage cell (TR-MC) population distinct in surface marker and transcriptional profile from circulating monocytes, dendritic cells, and tissue macrophages that are conserved in rheumatoid arthritis (RA) patients. TR-MCs are independent of NR4A1 and CCR2, long lived, and embryonically derived. TR-MCs undergo increased proliferation and reverse diapedesis dependent on LFA1 in response to arthrogenic stimuli and are required for the development of RA-like disease. Moreover, pathways that are activated in TR-MCs at the peak of arthritis overlap with those that are downregulated in LFA1 TR-MCs. These findings show a facet of mononuclear cell biology that could be imperative to understanding tissue-resident myeloid cell function in RA.
Topics: Humans; Monocytes; Synovial Membrane; Arthritis, Rheumatoid; Inflammation
PubMed: 37204925
DOI: 10.1016/j.celrep.2023.112513 -
Arteriosclerosis, Thrombosis, and... Jan 2021Atherosclerosis is characterized by incessant inflammation in the arterial wall in which monocytes and macrophages play a crucial role. During the past few years, it has... (Review)
Review
Atherosclerosis is characterized by incessant inflammation in the arterial wall in which monocytes and macrophages play a crucial role. During the past few years, it has been reported that cells from the innate immune system can develop a long-lasting proinflammatory phenotype after brief stimulation not only with microbial products but also endogenous atherogenic stimuli. This persistent hyperactivation of the innate immune system is termed trained immunity and can contribute to the pathophysiology of atherosclerosis. Trained immunity is mediated via epigenetic and metabolic reprogramming and occurs both in mature innate immune cells as well as their bone marrow progenitors. In addition to monocytes, other innate immune and nonimmune cells involved in different stages of atherosclerosis can develop comparable memory characteristics. This mechanism provides exciting novel pharmacological targets that can be used to prevent or treat cardiovascular diseases.
Topics: Animals; Atherosclerosis; Hematopoietic Stem Cells; Humans; Immunity, Innate; Immunologic Memory; Inflammation; Inflammation Mediators; Monocytes; Plaque, Atherosclerotic; Signal Transduction
PubMed: 33147995
DOI: 10.1161/ATVBAHA.120.314216 -
Aging Jan 2023
Topics: Monocytes; Lipopolysaccharide Receptors; Flow Cytometry
PubMed: 36645917
DOI: 10.18632/aging.204493 -
Frontiers in Immunology 2023Dendritic cells (DCs) play crucial roles in the pathogenesis of rheumatoid arthritis (RA), a prototypic autoimmune disease characterized by chronic synovitis and joint... (Review)
Review
Dendritic cells (DCs) play crucial roles in the pathogenesis of rheumatoid arthritis (RA), a prototypic autoimmune disease characterized by chronic synovitis and joint destruction. Conventional dendritic cells (cDCs) with professional antigen-presenting functions are enriched in the RA synovium. In the synovium, the cDCs are activated and show both enhanced migratory capacities and T cell activation in comparison with peripheral blood cDCs. Plasmacytoid dendritic cells, another subtype of DCs capable of type I interferon production, are likely to be tolerogenic in RA. Monocyte-derived dendritic cells (moDCs), once called "inflammatory DCs", are localized in the RA synovium, and they induce T-helper 17 cell expansion and enhanced proinflammatory cytokine production. Recent studies revealed that synovial proinflammatory hypoxic environments are linked to metabolic reprogramming. Activation of cDCs in the RA synovium is accompanied by enhanced glycolysis and anabolism. In sharp contrast, promoting catabolism can induce tolerogenic DCs from monocytes. Herein, we review recent studies that address the roles of DCs and their immunometabolic features in RA. Immunometabolism of DCs could be a potential therapeutic target in RA.
Topics: Humans; Arthritis, Rheumatoid; Synovial Membrane; Autoimmune Diseases; Monocytes; Dendritic Cells
PubMed: 37251399
DOI: 10.3389/fimmu.2023.1161148 -
Immunology May 2021When monocytes migrate from blood into tissues they differentiate into macrophage-like cells. The outcome of this differentiation process is strongly influenced by the...
When monocytes migrate from blood into tissues they differentiate into macrophage-like cells. The outcome of this differentiation process is strongly influenced by the tissue environment, and the macrophages produced help control the immunological properties of the tissue. The process of monocyte-macrophage differentiation is therefore potentially attractive when seeking therapeutic targets to amplify or modulate the inflammatory response. Here we highlight recent research in this area, identifying the gene Paqr11 as an important factor in monocyte differentiation, and therefore an important potential target for reducing macrophage-mediated inflammation in arthritis.
Topics: Cell Differentiation; Humans; Inflammation; Macrophages; Monocytes
PubMed: 33851416
DOI: 10.1111/imm.13334 -
Frontiers in Immunology 2019Tumor-associated macrophages (TAM) represent the main immune cell population of the tumor microenvironment in most cancer. For decades, TAM have been the focus of... (Review)
Review
Tumor-associated macrophages (TAM) represent the main immune cell population of the tumor microenvironment in most cancer. For decades, TAM have been the focus of intense investigation to understand how they modulate the tumor microenvironment and their implication in therapy failure. One consensus is that TAM are considered to exclusively originate from circulating monocyte precursors released from the bone marrow, fitting the original dogma of tissue-resident macrophage ontogeny. A second consensus proposed that TAM harbor either a classically activated M1 or alternatively activated M2 polarization profile, with almost opposite anti- and pro-tumoral activity respectively. These fundamental pillars are now revised in face of the latest discoveries on macrophage biology. Embryonic-derived macrophages were recently characterized as major contributors to the pool of tissue-resident macrophages in many tissues. Their turnover with macrophages derived from precursors of adult hematopoiesis seems to follow a regulation at the subtissular level. This has shed light on an ever more complex macrophage diversity in the tumor microenvironment than once thought and raise the question of their respective implication in tumor development compared to classical monocyte-derived macrophages. These recent advances highlight that TAM have actually not fully revealed their usefulness and deserve to be reconsidered. Understanding the link between TAM ontogeny and their various functions in tumor growth and interaction with the immune system represents one of the future challenges for cancer therapy.
Topics: Humans; Macrophages; Monocytes; Neoplasms; Tumor Microenvironment
PubMed: 31417566
DOI: 10.3389/fimmu.2019.01799