Articles tagged with Macrophages
A new study by the University of Nebraska-Lincoln has provided direct evidence that an algae-infecting virus can invade and replicate within some mammalian cells. The virus, known as Acanthocystis turfacea chlorella virus 1 (ATCV-1), successfully infiltrated macrophage cells in mice, causing changes characteristic of a viral infection.
A predictive model that measures invasiveness facilitated by macrophages from each individual donor has been developed to guide treatment options for breast cancer. The model correlates the level of invasion through a collagen gel to chemical signals expressed by macrophages, providing an invasiveness index for each patient.
Researchers find that using a monoclonal antibody to block the 'eat me' signal on malignant cells triggers a more potent immune response in dendritic cells, which then activate killer T cells and boost adaptive immunity. The study suggests a new approach for developing an effective cancer immunotherapy.
Researchers identified a pathway that leads to atypical blood vessel formation in age-related macular degeneration. Inhibiting this pathway may halt or restore sight in people with the disease.
A team of researchers from NTNU clarified a crucial step in the mechanism that allows mycobacteria to evade the immune system by hiding in macrophages. This finding adds to our understanding of the general mechanisms of how the immune system works, particularly in relation to inflammation and its regulation.
The tuberculosis bacterium co-opts mechanisms of the immune system to its own advantage by releasing small bits of DNA into macrophages. This triggers an immune response that helps the bacteria rather than fights it. Researchers have discovered a way to manipulate this process, potentially paving the way for new treatments
Researchers discovered a critical role of the body clock in controlling the immune response to infection. A microRNA called miR-155 helps stop the macrophage clock, allowing it to become inflamed, while restoring clock function may provide new therapies for inflammatory disorders.
Researchers found macrophages accumulate in different parts of the brain during HIV infection, leading to neurological damage. The study provides new insights into the timing and dynamics of white blood cell traffic in the central nervous system.
Researchers discovered that macrophages play an unexpected role in Rett syndrome, amplifying the disease instead of helping it. The study suggests modulating the immune system could delay symptom onset and slow disease progression.
Researchers discovered IRF5 helps prevent metabolic complications by storing fat subcutaneously. In contrast to intra-abdominal fat, which leads to type 2 diabetes, this storage form reduces inflammation and promotes tissue remodelling.
Researchers at the University of Virginia Health System identified a surprising contributor to Rett syndrome: immune cells bearing a mutated MeCP2 gene. These macrophages amplify disease progression by failing to maintain tissue homeostasis, highlighting the immune system as a promising therapeutic target.
Researchers at Ludwig-Maximilians-Universität München demonstrate that macrophages can effectively substitute for dendritic cells as primers of T-cell-dependent immune responses. They stimulate a more comprehensive immune reaction than cross-presenting dendritic cells, activating T-cells specific for all antigen-binding sites.
Researchers discovered that Salmonella lowers its cytoplasmic pH in response to acidic environments, triggering the secretion of virulence proteins. This low-pH signal activates an intracellular cascade that induces the formation of a nanomachine used for injecting virulence proteins into host cells.
A study led by researchers from Mount Sinai Hospital shows that a nanotherapeutic medicine can halt the growth of artery plaque cells and suppress inflammation, leading to reduced heart attack risk. The therapy uses high-density lipoprotein (HDL) to target inflamed immune cells in arterial plaques.
Research reveals vitamin D's role in preventing chronic inflammation that causes cardiometabolic disease, including type 2 diabetes and heart disease. Vitamin D helps immune cells reduce inflammation and prevent the formation of fat-laden macrophages.
Researchers discovered that macrophages activate the MAPK pathway, leading to increased tumor growth. Blocking this pathway reverses macrophage-mediated resistance and increases antitumor activity of BRAF inhibitors.
Scientists at ITMO University and their collaborators identified novel metabolic pathways controlling macrophage activation and its anti-inflammatory function. The study provides insights into the regulation of immune responses and may lead to the development of new drugs targeting macrophage metabolism.
Researchers at Stanford University School of Medicine have discovered a method to transform human leukemia cells into harmless immune cells called macrophages. This breakthrough offers potential hope for treating aggressive cancers like B-cell acute lymphoblastic leukemia.
Researchers found that deleting TREM2 receptor in mice with AD-like disease reduced plaque formation, brain inflammation, and improved neuron survival. Macrophages lacking TREM2 were more effective at clearing beta-amyloid aggregates, suggesting a potential role for the receptor in neurodegeneration.
A study published in the Journal of the American Society of Nephrology reveals a key signaling pathway that helps protect healthy tissue from excessive immune activation. This finding may lead to improved treatment options for patients with autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus.
Researchers at CNIO have discovered that macrophages, a type of immune cell, play a key role in activating hair follicle stem cells, promoting hair growth. This breakthrough could lead to the development of novel treatment strategies for hair loss and has broader implications for skin regeneration and cancer research.
A new study reveals that macrophages, a type of immune cell, play a crucial role in activating hair growth by surrounding and activating skin stem cells. This discovery may lead to the development of novel treatment strategies for hair loss in humans.
Researchers at Brunel University London found proteins that disguise nanoparticles, allowing them to target cancer cells without causing inflammation. This discovery has potential for treating inflammatory diseases like Parkinson's and Alzheimer's, and glioblastoma brain tumors.
A new study reveals that macrophages induce neutrophil reverse migration to resolve inflammation in wounds. Without macrophages, neutrophils remain in wounds longer, leading to recurring infections and exaggerated inflammation.
Researchers have discovered a receptor that can be activated by bile acids to reduce inflammation in fat tissue, which is associated with type-2 diabetes. This breakthrough could lead to the development of new anti-diabetes drugs.
Researchers found that macrophages, thought to be HIV's long-term hideout, are actually short-lived in primate model. The study suggests that therapeutic strategies targeting infected macrophages could facilitate viral elimination.
Researchers found that beneficial immune cells originate in the embryonic heart and can promote regeneration, while harmful macrophages come from the bone marrow. Blocking the influx of bone marrow-derived macrophages protects the resident macrophages, allowing them to promote repair and reduce inflammation.
Researchers developed stealthy nanoparticles that successfully deliver cancer vaccines to a subset of macrophages deep inside lymph nodes, hindering tumor growth. The nanoparticles bypass circulating immune cells and enter the lymph nodes' core, where they are engulfed by special kind of macrophage.
Researchers discover how stem cells combat lung disease by targeting macrophages, reducing inflammation and improving bacterial clearance. This breakthrough brings hope for new treatments for acute respiratory distress syndrome (ARDS) patients.
Researchers identified Maresin-Ls, molecules that promote wound healing and reduce inflammation in patients with diabetes. The study restores reparative functions to diabetic macrophages, enabling better treatment of diabetic wounds.
Researchers found that macrophages from the lungs of old mice had different responses to infections than those of young mice, but these changes were reversed by ibuprofen. The study suggests that reducing inflammation with diet, exercise, and/or drugs may help prevent or reduce diseases in the elderly.
Macrophages play a crucial role in regulating intestinal movements, and their interaction with the nervous system is adaptable to changes in the bacterial environment. The discovery may lead to new treatments for irritable bowel syndrome (IBS).
Researchers discovered how a protein molecule in immune cells promotes nitric oxide production, a potent weapon against bacterial attack. The discovery highlights the importance of finding a balance between fighting infection and preventing tissue damage.
Research discovered that glucose is the major nutrient used by Salmonella bacteria, but it's also able to use other nutrients. This finding informs potential therapeutic interventions to combat Salmonella infections. The study reveals a wealth of strategies employed by Salmonella to overcome host defenses and evade immune systems.
Researchers have identified a potential new class of nonsteroidal anti-inflammatory drugs that target the mPGES-1 enzyme, which reduces oxidative damage and slows atherosclerosis in macrophages. This could lead to safer pain relief options without increasing heart disease risk.
A Mount Sinai study reveals that GM-CSF protein production is critical for maintaining immune tolerance in the gut, and its deficiency may lead to increased susceptibility to inflammatory bowel diseases. The research suggests that targeting the GM-CSF axis could be a promising strategy for developing effective treatments for IBD.
Researchers at NYU Langone Medical Center discovered that blocking Netrin-1 stalls chronic inflammation and insulin resistance, a link between obesity and type II diabetes. The study found that Netrin-1 signaling promotes macrophage buildup in fat tissue, leading to inflammation and insulin resistance.
Researchers at NYU Langone Medical Center found that blocking the action of a key signaling molecule, Netrin-1, stalls chronic inflammation and insulin resistance tied to obesity. This could lead to further advances against diseases such as type II diabetes and atherosclerosis.
Researchers found a decrease in classical blood monocytes and an increase in CD14hiHLA-DRdim macrophages, which drive inflammation in the disease. This discovery may lead to new therapeutic targets for Crohn's disease treatment.
Dr. Gyorgy Fejer has developed a method to create continuously growing macrophage cells in the lab from mice, reducing the need for live animals in research. This could lead to significant reductions in animal usage and improve research effectiveness.
Immunologists at the University of Bonn have disproved a long-held classification of immune cells, finding that macrophages can take on multiple forms. This discovery offers new hope for treating diseases such as arthritis, diabetes, and cancer.
Researchers at the University of Bonn have decoded a new immunoregulatory mechanism controlling defense in urinary tract infections. The mechanism involves two types of macrophages regulating neutrophils, with sentinel macrophages triggering an alarm and helper macrophages providing a safety mechanism to prevent collateral damage.
Researchers found that macrophage populations actively phagocytose tumor cells following monoclonal antibody treatment. Optimized therapies may enhance macrophage recruitment and activity to improve removal of circulating tumor cells in cancer patients.
A study in mice reveals two major pools of immune cells that promote healing and drive inflammation in the heart. Healthy hearts maintain a population of embryonic macrophages, while adult macrophages are recruited during cardiac stress, leading to inflammation. The findings provide new insights into the complex interplay between these...
Researchers developed a novel sugar-based tracer contrast agent to aid in the detection of inflamed and vulnerable artery plaques. The new tracer, fluorodeoxymannose (FDM), shows promise in targeting high-risk plaques more specifically than traditional glucose-based tracers.
Researchers have discovered that indoleamine 2,3-dioxigenase (IDO) can promote inflammation in response to infection, potentially leading to new therapeutic targets. By manipulating IDO's activity, scientists may be able to fine-tune the immune response and reduce cytokine storms associated with severe infections.
Scientists have found that macrophages invade the diabetic pancreas, producing cytokines that contribute to insulin-producing beta cells' elimination. This discovery may lead to development of tailor-made anti-inflammatory therapies to reduce type 2 diabetes burden.
In a groundbreaking study, researchers found that benign E. coli bacteria can evolve to become pathogenic within 500 generations or 30 days when confronted with macrophages. The bacteria adapted by developing resistance to being killed by immune cells and acquiring traits similar to those of deadly pathogens.
VIB researchers have identified a protein, Nrp1, that suppresses the anti-tumor activity of macrophages. Blocking Nrp1 restores this immune response, leading to reduced tumor growth and improved prognosis.
Researchers have identified how golden staph bacteria target and destroy key immune cells, disrupting the body's defense against infection. By visualizing this process using advanced microscopy techniques, the team gained insights into how golden staph evades the immune system and causes tissue damage.
Researchers discovered that S. aureus converts neutrophil extracellular traps into a toxic molecule, dAdo, which kills macrophages and allows the bacteria to avoid immune destruction. The study provides new insights into the mechanisms behind S. aureus infections and offers potential therapeutic targets.
A dysfunctional chemokine receptor, CXCR1, plays a crucial role in Candida infection progression. Mice lacking this receptor are prone to kidney failure due to Candida-induced injury. Additionally, patients with a mutation in the CXCR1 gene are at higher risk of developing candidiasis.
Researchers from Imperial College London have discovered how Mycobacterium tuberculosis tricks the immune system to establish persistent infections. They hope to develop small molecule drugs that can block or destroy the bacteria by targeting these sugar molecules.
A new study from Japan found that individuals with a history of kidney stones have significantly increased levels of inflammatory chemokines GRO and CXCL1, while those without kidney stones have higher levels of anti-inflammatory cytokine IL-4. This research may lead to the development of new therapeutic drugs for kidney stone formation.
Researchers at the University of Washington have developed a method to target and eliminate harmful macrophages that dampen the immune response to cancer. By depleting these 'traitor' immune cells, tumor growth is slowed and survival rates are improved in mice with cancer.
The researcher aims to establish permanently growing, alternatively activated M2 macrophage cell lines to reduce animal use in studies. This innovation could provide scientists with almost limitless cells for study without the need for live mice.
Salmonella bacteria can manipulate macrophages to switch from an inflammatory to anti-inflammatory state, promoting chronic asymptomatic carriage of typhoid fever. This mechanism could lead to new treatments for typhoid fever, a disease that causes hundreds of thousands of deaths each year.
A new study from the University of Toronto and Massachusetts General Hospital found that macrophage growth inside arterial plaques is not reliant on external cells. This discovery may lead to alternative approaches to treating atherosclerosis, a leading cause of cardiovascular disease.
Researchers at Massachusetts General Hospital found that macrophage proliferation within plaques drives the growth of atherosclerotic lesions. This challenges the previous assumption that monocytes are solely responsible for plaque development.
Researchers at Caltech have discovered a new mechanism for creating macrophages by increasing the accumulation of regulatory protein PU.1 through slowed cell division. The process involves an unexpected cycle where cell division slows, allowing higher PU.1 levels to accumulate and prompt macrophage generation.