Modulation of macrophage activation state protects tissue from necrosis during critical limb ischemia in thrombospondin-1-deficient mice.. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Home » Type i IFN inhibits alternative macrophage activation during mycobacterium tuberculosis infection and leads to enhanced protection in the absence of IFN-γ ...
Summary: Activated macrophages and their inflammatory products play a key role in innate immunity and in pathogenesis of autoimmune/inflammatory diseases. Macrophage activation needs to be tightly regulated to rapidly mount responses to infectious challenges but to avoid toxicity associated with excessive activation. Rapid and potent macrophage activation is driven by cytokine-mediated feedforward loops, while excessive activation is prevented by feedback inhibition. Here we discuss feedforward mechanisms that augment macrophage responses to Toll-like receptor (TLR) ligands and cytokines that are mediated by signal transducer and activator of transcription 1 (STAT1) and induced by interferon-γ (IFN-γ). IFN-γ also drives full macrophage activation by inactivating feedback inhibitory mechanisms, such as those mediated by interleukin-10 (IL-10), and STAT3. Priming of macrophages with IFN-γ reprograms cellular responses to other cytokines, such as type I IFNs and IL-10, with a shift toward ...
TY - JOUR. T1 - Involvement of complement in B-cell, T-cell and monocyte/macrophage activation. AU - Dierich, M. P.. AU - Erdei, A.. AU - Huemer, H.. AU - Petzer, A.. AU - Stauder, R.. AU - Schulz, T. F.. AU - Gergely, J.. PY - 1987/2. Y1 - 1987/2. N2 - In the early 70s it had been shown, that for the immune response against T-dependent antigens C3 was necessary, while T-independent antigens, although activating the alternative pathway of complement, triggered antibody formation also in C-deficient mice. During recent years functional and biochemical knowledge about complement binding structures on B-cells and monocytes/macrophages continuously increased and, also, on T-cells C3 binding entities have been detected. In the case of B-cells and, at least in special experimental conditions, in the case of T-cells C3 can exert a proliferative response as long as the cells are prestimulated (excited) by anti-Ig or IL-2, respectively. Monocytes can bind C3b- or iC3b-carrying particles, but only when ...
In the present study we show that, in the mouse model of aseptic lung injury, macrophages first exhibit a proinflammatory M1 phenotype, followed by an M2 anti-inflammatory phenotype. Genetic ablation of Akt2 suppresses M1 activation via miR-146a induction, promotes an M2 phenotype, and protects mice from acid-induced lung injury.. ARDS, the devastating clinical syndrome of acute respiratory failure characterized by lung inflammation and alveolar barrier dysfunction, is a major cause of morbidity and mortality in patients in the intensive care unit. Although pneumonia and sepsis are the most common causes of ARDS, several aseptic conditions are associated with ARDS, such as acute pancreatitis, burns, near drowning, multiple trauma, and inhalation injury (1). With no effective treatment available, there is an urgent need to understand and, subsequently, modulate the pathogenesis of lung inflammation.. It is well established that macrophages play a central role in the pathogenesis of ARDS (4, 5, ...
Macrophages are found in most tissues of the body, where they have tissue- and context-dependent roles in maintaining homeostasis as well as coordinating adaptive responses to a variety of stresses. Their capacity for specialized functions is controlled by polarizing signals, which activate (or polarize) macrophages by upregulating transcriptional programs that encode distinct effector functions. An important conceptual advance in the field of macrophage biology, emerging from recent studies, is that macrophage activation is critically supported by metabolic shifts. Metabolic shifts fuel multiple aspects of macrophage activation, and preventing these shifts impairs appropriate activation. These findings raise the exciting possibility that macrophage functions in various contexts could be regulated by manipulating their metabolism. Here we review the rapidly evolving field of macrophage metabolism, discussing how polarizing signals trigger metabolic shifts and how these shifts enable appropriate
Description of macrophage activation is currently contentious and confusing. Like the biblical Tower of Babel, macrophage activation encompasses a panoply of descriptors used in different ways. The lack of consensus on how to define macrophage activation in experiments in vitro and in vivo impedes p …
Curine is a bisbenzylisoquinoline alkaloid (BBA) with anti-allergic, analgesic, and anti-inflammatory properties. Previous studies have demonstrated that this alkaloid is orally active at non-toxic doses. However, the mechanisms underlying its anti-inflammatory effects remain to be elucidated. This work aimed to investigate the effects of curine on macrophage activation and neutrophil recruitment. Using a murine model of lipopolysaccharide (LPS)-induced pleurisy, we demonstrated that curine significantly inhibited the recruitment of neutrophils in association with the inhibition of cytokines tumor necrosis factor (TNF-α), interleukin (IL)-1β, IL-6, monocyte chemotactic protein (CCL2/MCP-1) as well as leukotriene B4 in the pleural lavage of mice. Curine treatment reduced cytokine levels and the expression of iNOS in in vitro cultures of macrophages stimulated with LPS. Treatment with a calcium channel blocker resulted in comparable inhibition of TNF-α and IL-1β production, as well
TY - JOUR. T1 - Heterogeneity of macrophage activation in anti-Thy-1.1 nephritis. AU - Minto, A.. AU - Erwig, Lars Peter. AU - Rees, Andrew Jackson. PY - 2003/11. Y1 - 2003/11. N2 - Macrophages infiltrating glomeruli in telescoped nephrotoxic nephritis are programmed. The purpose of this study was to assess whether macrophages infiltrating glomeruli of rats with passively induced injury become similarly programmed, and to determine whether macrophage commitment is an early event. Glomerular macrophages isolated from rats with resolving and proliferative anti-Thy-1 nephritis were examined for nitric oxide (NO) generation and expression of lysosomal hydrolases. After a single injection of Thy-1 antibody the cells generated large amounts of NO that was attenuated ex vivo by transforming growth factor-beta and other anti-inflammatory cytokines. In contrast macrophages infiltrating glomeruli immediately after a second injection of Thy-1 antibody generated No spontaneously and were unresponsive to ...
Several computationally predicted activating metabolic substrates are well established to be critical for macrophage activation (Figure 2). Oxygen, glucose, and glutamine have all been previously shown to be of great importance in macrophage metabolism and activation as they are key for cellular respiration, energy production, and respiratory burst (Newsholme et al, 1996). High consumption of glutamine is particularly important for enhancing immunity (Newsholme et al, 1999), as it is required for arginine biosynthesis and nitrite/urea production (Murphy and Newsholme, 1998). The uptake of arginine and the branched chain amino acids (BCAAs) valine and isoleucine were also identified to be important for ATP, NADH, proline, and putrescine production; however, it was not found to be critical for NO production. Arginine is among the most critical amino acid as it is a direct precursor metabolite for NO (Baydoun et al, 1993) and its transport increases up to five‐fold during activation and ...
Boraschi, D; Soldateschi, D; and Tagliabue, A, "Macrophage activation by interferon: dissociation between tumoricidal capacity and suppressive activity." (1982). Subject Strain Bibliography 1982. 2304 ...
Room 4137 Aloke Virmani Finn, MD Associate Professor of Medicine, University of Maryland Alternative Macrophages, Angiogenesis, and Plaque Progression in Atherosclerosis
Macrophages are extremely versatile cells, distributed throughout all tissues, involved in numerous functions, and equipped with many sensing receptors and effector molecules
Carol Ho Yan Fong, Magali Bebien, Arnaud Didierlaurent, Ruth Nebauer, Tracy Hussell, David Broide, Michael Karin, Toby Lawrence ...
The proposal intends to advance both novel statistical methods for genomic research and discoveringcomplex molecular mechanisms on the teratoma initiation and p...
ZC3H12B, 0.1 mg. ZC3H12B, also known as MCPIP2, is a member of a family of novel CCCH-zinc finger proteins that regulate macrophage activation and may be involved in host immunity and inflammatory diseases.
It may be hard to resist their little paws, ringed tails and bandit masks, but feeding those begging raccoons is a recipe for disaster, wildlife experts say.
Definition of macrophage-activating factor in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is macrophage-activating factor? Meaning of macrophage-activating factor as a legal term. What does macrophage-activating factor mean in law?
Although macrophage activation is a necessary component of host defense, if left uncontrolled it can lead to tissue damage, organ failure, and even death. Prolonged macrophage activation has been associated with an extensive list of chronic inflammatory diseases, such as inflammatory bowel disease, rheumatoid arthritis, and a variety of macrophage activation syndromes (9, 18). However, the molecular mechanisms governing the regulation of macrophage activation under these pathologic conditions remains incompletely understood. In this study, we reveal a novel mechanism wherein IFN-γ interferes with the macrophages intrinsic ability to control its activation state, and demonstrate that IFN-γ actively desensitizes macrophages to immunosuppressive adenosine, thereby sustaining inflammatory responses.. This work demonstrates that IFN-γ inhibits a recently described purinergic autoregulatory loop that is initiated upon TLR ligation of macrophages. We previously demonstrated that macrophages secrete ...
Results Natural anti-oxLDL IgM monoclonal antibody 3A6 specifically inhibited the binding of CuoxLDL to naïve macrophages in vitro. 3A6 failed to inhibit the binding of CuoxLDL to LPS-activated macrophages and promoted the formation of CuoxLDL-mediated foam macrophages. Furthermore, 3A6 F (ab′)2 or pre-incubation with un-related IgM inhibited the binding of 3A6/CuoxLDL complex to LPS-activated macrophages, suggesting that the Fcα/μ receptor may be responsible for the binding of 3A6/CuoxLDL complex to LPS-activated macrophages. Indeed, LPS up-regulated the expression of Fcα/μ receptor in macrophages in a dose- and time-dependent manner, which was diminished by treatment with anti-TLR4 neutralising mAb. In addition, LPS induced the phosphorylation of p38MAPK and translocation of NF-kB p65, contributing to the up-regulated expression of Fcα/μ receptor in macrophages as treatment with specific inhibitor for p38MAPK (SB203580) or NF-kB (PDTC) attenuated the up-regulation of Fca/m receptor ...
Macrophage-Activating Factors: Factors secreted by stimulated lymphocytes that prime macrophages to become nonspecifically cytotoxic to tumors. They also modulate the expression of macrophage cell surface Ia antigens. One MAF is INTERFERON-GAMMA. Other factors antigenically distinct from IFN-gamma have also been identified.
It is widely known that macrophages can be activated to kill tumor cells. It is also known that tumor-infiltrating macrophages can be immunosuppressed. The mechanisms of both tumor killing by activated macrophages and tumor-induced macrophage suppression are not entirely clear. To better understand the mechanisms that macrophages use to kill tumor cells, a murine macrophage cell line, RAW264.7, was fixed with paraformaldehyde, subsequently stimulated with lipopolysaccharide (LPS) and co-cultured with tumor cells. Macrophage activity was assessed by nitric oxide (NO) production and tumor cell growth inhibition in the 3H-thymidine incorporation assay. It was found that fixed macrophages were still able to suppress the proliferation of tumor cells while the production of NO was abrogated. Additionally, a model of tumor-induced suppression of macrophages was developed by co-culturing them with tumor cell conditioned media before adding LPS. Inhibition of macrophage activity by tumor cell products ...
Macrophages are usually found in tumor infiltrates where they exert cytostatic/cytotoxic activities against tumor cells. The tumoricidal activity is enhanced by activation of macrophages with bacterial products or cytokines (1,2). Recently nitric oxide (NO) has been indicated as a critical effector molecule for macrophage anti-tumor activity (3,4). Macrophages can be induced to release NO upon stimulation with a variety of stimuli such as bacterial products or cytokines (3,5). More recently it has been reported that mycoplasma-treated macrophages release large amounts of NO (6).. YAC-1 tumor cells have been classically used as targets for natural killer (NK) cells. Resident macrophages do not present anti-YAC-1 activity, but lymphokine-activated macrophages are able to kill YAC-1 cells (7). The mechanism by which lymphokine-activated macrophages kill YAC-1 cells remains unsettled.. Based on these observations, we asked whether mycoplasma-infected YAC-1 tumor cells could stimulate macrophages to ...
Polarization has been a useful concept for describing activated macrophage phenotypes and gene expression profiles. However, macrophage activation status within tumors and other settings are often inferred based on only a few markers. Complicating matters for relevance to human biology, many macrophage activation markers have been best characterized in mice and sometimes are not similarly regulated in human macrophages. To identify novel markers of activated human macrophages, gene expression profiles for human macrophages of a single donor subjected to 33 distinct activating conditions were obtained and a set of putative activation markers were subsequently evaluated in macrophages from multiple donors using integrated fluidic circuit (IFC)-based RT-PCR. Using unsupervised hierarchical clustering of the microarray screen, highly altered transcripts (>4-fold change in expression) sorted the macrophage transcription profiles into two major and 13 minor clusters. Among the 1874 highly altered transcripts,
Macrophages display remarkable plasticity, with the ability to undergo dynamic transition between different functional phenotypes.63,64 Macrophages activated by TLR ligands and IFN-γ are called M1 macrophages (also referred to as classically activated macrophages).63-65 Conversely, stimulation of macrophages with Th2 cytokines, such as IL-4 or IL-13, immune complexes plus TLR ligands, IL-10, transforming growth factor-β, or glucocorticoids induces the generation of M2-type macrophages (also called alternatively activated macrophages).63-65 M1 macrophages produce high amounts of proinflammatory cytokines and NO by expressing inducible NO synthase and are important for eradicating bacterial, viral, and fungal infections.63-65 M2 macrophages are characterized by their high expression of markers of alternative activation, such as arginase-1, Chitinase 3-like 3 (also called YM-1), and found in inflammatory zone 1 (FIZZ1), and regulate responses to parasite infection, tissue remodeling, ...
Immortalized Murine Macrophage Cell Line as a Model for Macrophage Polarization into Classically Activated M(IFNγ+LPS) or Alternatively Activated M(IL-4) Macrophages Abstract.
The regulation of macrophage activator protein-1 (AP-1) gene expression by LPS and cytokines is of potentially crucial importance in the pathogenesis of several diseases. The action of LPS and four cytokines on AP-1 gene expression in the murine macrophage J774.2 cell line was, therefore, studied. Exposure of the cells to IL-6 produced no changes in the mRNA levels of all AP-1 members studied. In contrast, the expression of JunB, c-jun and c-fos, but not JunD, was increased by LPS, TNF-α, IFN-γ and IL-1, albeit with different kinetics and magnitude of induction. Electrophoretic mobility shift assays showed a close correlation between the expression of the AP-1 genes and the functional AP-1 DNA binding activity and, additionally, demonstrated the participation of heterodimeric interactions between the different members. These studies provide insights into the potential mechanisms that may be involved in the mediator-specific modulation of AP-1 regulated macrophage gene expression.. ...
Scientific background: Activated macrophages, present in excess during natural inflammatory responses, bear the potential to kill and eradicate cancer cells. Efranat has developed cancer immunotherapy based on macrophage activation using a plasma protein designated EF-022, a modified Vitamin D Binding Protein Macrophage Activator.. Methods: We performed an open label single-center phase I study in patients diagnosed with inoperable, recurrent or metastatic malignant solid tumors, deemed incurable, and who have failed to respond to standard therapy or for whom no standard therapy is available. The dose-escalation study was comprised of three cohorts, each receiving intramuscular (IM) injections of EF-022, once weekly for two cycles of treatment. Each cycle consisted of 4 weekly injections. Three dose levels were evaluated: 100 ng, 500ng and 1000ng. Patients were followed for up to 12 months from the start of treatment. The primary study objectives were to determine the safety and tolerability and ...
When deprived of oxygen, Bacille Calmette-Guérin (BCG)-activated macrophages no longer lysed P388 lymphoma cells. Both H2O2 release and cytotoxicity by BCG-activated macrophages and by granulocytes triggered with phorbol myristate acetate (PMA) were markedly inhibited when the glucose concentration in the medium was reduced to 0.03 mM or less, or if glucose were replaced with galactose. Catalase abolished PMA-triggered cytotoxicity by both types of effector cells, whereas superoxide dismutase had no effect. Ferricytochrome C reduced the cytotoxicity of BCG-activated macrophages, an effect which was largely reversed by superoxide dismutase. 10 drugs, thought to quench singlet oxygen and/or scavenge hydroxyl radical, did not affect cytotoxicity in this system. Neither azide nor cyanide reduced cytolysis, but there was marked inhibition by lactoperoxidase and iodide. This suggested that cytotoxicity was not dependent upon myeloperoxidase, and that lactoperoxidase may have diverted H2O2 from the ...
Stinnett, J D.; Morris, M J.; and Alexander, J W., "Macrophage activation and increased resistance to infection in immunosuppressed mice treated with corynebacterium parvum vaccine or pyran copolymer." (1979). Subject Strain Bibliography 1979. 484 ...
In our bitransgenic mouse model, we demonstrate that hypoxia provokes an accumulation of alternatively activated alveolar macrophages that precedes the development of pulmonary hypertension and appears to play a critical role in the pathogenesis of disease. Overexpression of HO-1 induced a switch in macrophage polarity toward an anti-inflammatory phenotype, and this effect was associated with protection from HPH.. Hypoxia resulted in alveolar inflammation that consisted predominantly of macrophages. These findings correlate with the fact that macrophages tend to accumulate in poorly vascularized areas with low oxygen tension,29 and correlates with previous studies in HPH that highlighted the predominant role of the monocyte/macrophage lineage in modulating vascular remodeling.8 Additionally, we found that hypoxia in vivo and in vitro polarized the population of alveolar macrophages toward the M2 phenotype. Hypoxic microenvironment is also a hallmark feature of tumors, and similar to the hypoxic ...
Macrophages are plastic and versatile cells adapting their function/phenotype to the microenvironment. Distinct macrophage subpopulations with different functions, including classically (M1) and (M2) activated macrophages, have been described. Reciprocal skewing of macrophage polarization between the M1 and M2 state is a process modulated by transcription factors, such as the nuclear peroxisome proliferator-activated receptors. However, whether the estrogen/estrogen receptor pathways control the balance between M1/M2 macrophages is only partially understood. Estrogen-dependent effects on the macrophage system may be regarded as potential targets of pharmacological approaches to protect postmenopausal women from the elevated risk of cardiovascular disease.. ...
Possibly by assuring PETA that the only reason they were doing this was to save the animals from the summer heat, the authors of this paper exposed mice to the cold by sticking them into cages that had been pre-chilled to 4°. They saw that in BAT and WAT specifically, macrophages were activated in the alternative manner rather than the classical. Through gene expression analysis and flow cytometry, they saw that whereas the genes for alternative activation were progressively increased as the temperature was decreased, the genes for the classical activation were unchanged. Correspondingly, when Nguyen, et al. looked at mice that do not have the IL-4 and IL-13-and so, mice that did not have any choice but to activate macrophages through the classical pathway, they did not see the same increase in gene expression in these mice. They also made sure that this increase in alternative activation was specific to the BAT and WAT by looking for the same reactions in other tissues, including skeletal ...
Macrophages were first identified by Elie Metchnikoff more than a century ago as cells essential for host defense. Despite the fact that macrophages are one of the oldest immune cells known to man, this field is currently undergoing a thrilling revival as recent technological advances have revealed the fascinating diversity of macrophages and their essential functions in tissue homeostasis, wound healing, morphogenesis, cancer and metabolism. Importantly, it is now clear that macrophages in inflamed tissues comprise distinct subsets that differ in cellular origin and functional specialization.. This complexity has forced researchers to develop new tools to study the role of these intriguing cells in health and disease. Technological advances now permit the transcriptomic profiling and precise tissue localization of macrophages at the single-cell level, but these advances also bring puzzling questions regarding the inter- and intracellular networks that control macrophage function.. To help meet ...
Macrophages play an important role in the antitumour activity of photodynamic therapy. Preclinical studies in mice demonstrated a significant enhancement in the
Macrophage polarization review exploring the function and phenotype of M1, M2, TAM, TCR+, CD169+ macrophages, plus comparisons between mouse and human macrophages
Regularly, we identified that host macrophages engulfed alloreactive T cells in between and h of in vitro culture and, as a result, way more effectively than host DC . To examine regardless of whether host macrophages may also engulf donor T cells in vivo, we traced the fate of alloreactive T cells for the duration of the h just after their injection in lethally irradiated recipient mice. Alloreactive T cells accumulated close to the spleen marginal zone shortly after adoptive transfer and steadily shifted toward the T cell area . A substantial amount of donor T cells had been trapped in the red pulp in close contact with host macrophages at early time points after their transfer . Steady with effects obtained in cultures, CFSE labeled donor T cells have been engulfed by splenic macrophages in the course of the 1st day of transplant and ahead of the initiation of donor T cell proliferation in vivo ...
Although caspase-8 is a well-established initiator of apoptosis and suppressor of necroptosis, recent evidence suggests that this enzyme maintains functions beyond its role in cell death. As cells of the innate immune system, and in particular macrophages, are now at the forefront of autoimmune disease pathogenesis, we examined the potential involvement of caspase-8 within this population. Cre LysM Casp8 fl/fl mice were bred via a cross between Casp8 fl/fl mice and Cre LysM mice, and RIPK3 −/− Cre LysM Casp8 fl/fl mice were generated to assess the contribution of receptor-interacting serine-threonine kinase (RIPK)3. Immunohistochemical and immunofluorescence analyses were used to examine renal damage. Flow
Monoclonal antibody (MAB) therapies targeting central mediators of inflammatory responses, such as TNFα, have become a common immunotherapy approach in contemporary clinical practice. Unfortunately, TNFα MAB therapy comes at a cost of significantly increased risk for the development of devastating infections (22-24, 34). Following our previous work, which established the central role of TNFα for the development of protective TH1 immunity in the relevant model of IFI (7, 25, 26, 35), here, we defined a previously unknown mechanism by which TNFα exerts its profound and lasting effect on host defenses. We provide evidence that (i) TNFα contributes to the generation of a uniquely stable DC1 phenotype, which is resistant to DC2 repolarization; (ii) TNFα-stabilized DCs arising during the afferent phase of the immune response are required for generation and sustenance of protective TH1/TH17 immunity; (iii) TNFα-mediated DC1 stabilization is associated with the H3K4me3 histone modification at ...
The most abundant immune cell types of the tumor microenvironment macrophages recruited there by tumor-eluted factors. The role of these immune cells in tumor progression, and the interplay between tumor and immune cells is an emerging field of research with potential for novel treatment strategies. Here, a TIE2 expressing macrophage (TEM) subtype is integrated into a virtual tumor model. Within the 2D microenvironment, the TEM will differentiate from an extravasated monocyte precursor, congregate around the abluminal side of the vasculature in response to a chemoattractant gradient, secrete cytokines which favor differentiation of a separate angiogenic macrophage subtype [1]. The effects of macrophage populations on tumor progression on angiogenic activity and tumor growth will be examined.
The purpose of my talk was to discuss the biology of some of the immunotherapies as they apply to myeloma. So the focus was actually on therapies that manipulate how T-cells are activated and how they are directed. I spoke about immune checkpoints and agonists; I touched on vaccines and I also briefly touched on CAR T-cell therapy as well.. Could you tell us more?. Ill start with the immune checkpoints and agonists. So these are a family of molecules that regulate how T-cells function once they see an antigen. The prototype molecules in this family are CTLA4 which is an intrinsic mechanism by which T-cell activation is turned off. The other type of molecule that is probably much better known is PD-1. Both of these molecules get upregulated on T-cells once their activation programme is initiated and they are mechanisms of intrinsic T-cell self-regulation that occurs. Blocking these pathways is beneficial for cancer immunotherapy; there has been, particularly with PD-1 pathway blockade, both ...
Networksdisplay a set of signaling pathways, transcriptional and posttranscriptional regulation of M1/ M2 macrophage polarization.
Macrophages are important cells at the front-line of immunity where one of their main roles is to release anti-bacterial proteins. We will study the macrophage molecules, subcellular organelles and pathways that help to release these proteins to kill backteria and fight infection. Our studies will identify new cellular targets for boosting immunity and treating inherited diseases with defective macrophage function ...
This page is for a 20.109 project by Katie and Emily. Our initial idea is to use macrophage therapy to target Tay Sachs disease. We would transfect macrophages with CRIPSR machinery, designed to make 2 double stranded breaks around the mutated hexosaminidase A gene and have a donor dsDNA with the correct version of the gene homologously recombine with the genome. Macrophages are good at crossing the blood brain barrier and are known to transport their genetic material in exosomes efficiently to target cells. Macrophages are also naturally produced by humans, limiting immune response associated with other gene delivery methods such as viruses. Tay Sachs disease already has a substantial animal model since the genomic locus at which the mutation occurred is known. CRISPRs are also the latest genome editing technology, but have yet to come near clinical trials. ...
AB0069 TIE2 signalling induces a pro-inflammatory and pro-angiogenic phenotype in differentiated macrophages, independently of macrophage polarization conditions ...
TY - JOUR. T1 - Electric fields. T2 - a novel non-chemical regulator of human macrophage function. AU - Hoare, J. I.. AU - Barker, R. N.. AU - Mccaig, C. C.. AU - Rajnicek, A.. AU - Wilson, H. M.. PY - 2014/12. Y1 - 2014/12. U2 - 10.1111/imm.12406. DO - 10.1111/imm.12406. M3 - Abstract. VL - 143. SP - 96. EP - 96. JO - Immunology. JF - Immunology. SN - 0019-2805. IS - Suppl 2. M1 - 291. ER - ...
Defining the origins and developmental pathways of tissue-resident macrophages should help refine our understanding of the role of these cells in various disease settings and enable the design of novel macrophage-targeted therapies. In recent years the long-held belief that macrophage populations in …
: macrophages cultured with mouse serum (MS) have a different morphologyappearance, higher number of vesicle-like organelles and greater area.Macrophages cultur
Sigma-Aldrich offers abstracts and full-text articles by [Mikel Aristorena, Francisco J Blanco, Mateo de Las Casas-Engel, Luisa Ojeda-Fernandez, Eunate Gallardo-Vara, Angel Corbi, Luisa M Botella, Carmelo Bernabeu].
Macrophages are tissue-resident or infiltrated immune cells critical for innate immunity, normal tissue development, homeostasis, and repair of damaged tissue. Macrophage function is a sum of their ontogeny, the local environment in which they reside, and the type of injuries or pathogen to which they are exposed. In this Review, we discuss the role of macrophages in the restoration of tissue function after injury, highlighting important questions about how they respond to and modify the local microenvironment to restore homeostasis.. ...