Articles tagged with Macrophages
PARP9 and PARP14 have been identified as regulators of macrophage activation, a key factor in the development of atherosclerosis. The study found that silencing these genes had opposite effects on macrophage activation, with PARP14 increasing and PARP9 decreasing activation.
Researchers found that removing aging macrophages from atherosclerosis-prone mice reduced plaque buildup by 60%, suggesting a potential cellular target for therapy. The study also showed that suppressing senescence limited disease progression and reduced markers of plaque instability.
The study demonstrates the effectiveness of activity-based probes in detecting early signs of atherosclerosis. By targeting cysteine cathepsins, the probes image activated macrophage populations using optical and PET/CT methods, providing real-time monitoring of disease progression and therapeutic responses.
Researchers found that manipulating macrophages' metabolism can prevent tumor cells from spreading by stealing glucose, leading to a structured vessel barrier. The study's findings may lead to new cancer therapies targeting mTOR inhibitors and improving treatment outcomes for patients.
A significant proportion of macrophages are distributed to tissues before bone marrow function starts, maintaining themselves through stem cell-like renewal. Embryonic-derived macrophages regulate iron metabolism and the growth of the mammary gland in adults.
Tumor cells attract macrophages by releasing cytokines, which secrete growth factors that help tumor cells form spheroids and grow. Inhibiting these growth factors reduces tumor cell proliferation in a mouse model of ovarian cancer. This study sheds light on the early stages of ovarian tumor metastasis.
Macrophages can differentiate between infections and tissue injury using a single sensor, deploying specific immune responses. This discovery could lead to new targets for treating diseases with extensive tissue damage like arthritis or cancer.
Macrophages have been shown to play a crucial role in enthesitis, inflammation of tendons. Researchers found that blocking JAK inhibitors can prevent the increase of STAT1 and successfully treat Achilles enthesitis. This discovery may offer new treatment options for patients with inflammatory rheumatic diseases.
Researchers found that Zika virus productively infects primary human placenta-specific macrophages, with 10-15% of placental macrophages infected. The study suggests that placental macrophages may play a role in maternal-fetal Zika transmission and warrants further investigation.
A team of researchers found that a subset of macrophage cells in the heart produce molecules attracting neutrophils. Loss of these macrophages or blocking their production reduces neutrophil migration to the injured area. The study suggests resident macrophages provide signals calling neutrophils to the site.
Researchers at Drexel University discovered that a specific type of ceramic scaffold causes macrophages to transform into an M2c phenotype, promoting bone regeneration. Direct contact between macrophages and scaffolds is essential for this process.
Researchers identify CD47 protein in atherosclerotic plaques, which enables immune system to evade clearing dead cells, leading to plaque buildup and cardiovascular disease. Anti-CD47 antibodies show promise in preventing plaque formation and regression in mouse models.
A recent study reveals that ship engine emissions adversely affect macrophages, a key component of the immune system. The toxic effects of these emissions on macrophages can lead to pro-inflammatory reactions and other biological processes, highlighting the need for efficient particle-reducing measures.
Researchers at the University of Basel have identified a protein called gasdermin D that drives immune cells to pyroptosis, a form of programmed cell death. This process allows macrophages to burst open and expose pathogens, which can then be targeted by the immune system.
Scientists discovered that itaconate, a natural substance produced by macrophages, acts as an antioxidant and anti-inflammatory agent. It reduces the activity of immune cells and may be used to treat pathologies caused by excessive inflammation or oxidative stress.
A study published in Circulation found that increasing IGF-1 levels in macrophages could reduce plaque buildup and lower the risk of heart disease in older adults. Higher IGF-1 levels were associated with less plaque buildup and more stable plaques.
Researchers at EPFL have found a way to reclaim corrupted immune cells and turn them into signals for the immune system to attack tumors. They identified a molecular switch that can convert hijacked macrophages into cells stimulating the immune system to fight cancer growth and spread.
Researchers found that electrical fields enhanced macrophage migration and phagocytosis, cleaning the wound site and boosting healing ability. This discovery may have wide-reaching implications for diseases where macrophages play a role.
Researchers discovered that macrophages can grab and repair broken blood vessel ends in zebrafish brains, suggesting a potential natural repair mechanism for microbleeds. This process, observed over three hours, involved adhesion molecules and mechanical traction forces.
A study by Ken Suzuki and team found that M2 macrophages play a crucial role in repairing damaged myocardial tissue after a heart attack. Supplementing with these cells or using the cytokine IL-4 can restore repair capabilities and potentially reduce the risk of cardiac rupture.
A new USC study has found that mother's hepatitis B can support chronic infection in children, leading to a potential cure. The research, published in Immunity journal, suggests that removing 'traitor' cells from the liver's immune system may be key to clearing the virus.
A recent study discovered that macrophages in abdominal cavities surrounding organs like the liver and heart can initiate immediate and rapid repair after damage. The study found that these immune cells patrol within the cavity and adhere to damaged areas for quick healing, suggesting a new approach to tissue repair.
Removing osteopontin from mice with muscular dystrophy reduces inflammation and fibrosis, boosting muscle repair and regeneration. Osteopontin inhibitors may be used to slow disease progression and improve muscle function in DMD patients.
Researchers at Massachusetts General Hospital identified subcapsular sinus macrophages that form a protective barrier around lymph nodes, blocking the spread of melanoma and other cancers. These SCS macrophages act as tumor suppressors but can be disrupted by cancer treatment drugs.
Researchers developed nanoparticles that target CD98, a glycoprotein promoting inflammation in IBD. These particles showed anti-inflammatory capacity without toxicity, offering an alternative treatment to existing medications.
Researchers have found that CD163 can predict mortality in blood samples from patients with acute on chronic liver failure, a condition with a high four-week mortality rate of 20-30%. Measuring this biomarker may lead to improved diagnostics and treatment towards macrophages via CD163.
Research reveals that smoking damages macrophages, leading to TB infection and worsening its progression. The impaired cells can't recycle debris, becoming 'clogged up' and less effective at fighting infection.
Macrophages produce antimicrobial substances and fatty acids during activation to combat pathogens, contrary to previously assumed metabolism. The study provides a new approach for treating chronic inflammatory diseases by targeting the production of pyruvate in the citric acid cycle.
Researchers found that HIV-infected adolescent males had increased levels of sCD14, a marker of macrophage activation, leading to lower bone mass and density. This is due to the protective effects of estrogen in females, which represses macrophage function.
Researchers at UNC School of Medicine have demonstrated that HIV infects and replicates in macrophages, a discovery with significant implications for HIV cure research. The study found that macrophages can sustain HIV replication in the absence of T cells and can establish infection in new hosts.
Scientists designed a novel bispecific antibody that selectively blocks overproduction of TNF, a protein harmful when overproduced in autoimmune diseases. The prototype shows promise for treating conditions such as rheumatoid arthritis and Crohn's disease.
Researchers have discovered a novel role for CD40 antibodies in re-educating macrophages to break down the tumor microenvironment, allowing chemotherapy to target pancreatic cancer more effectively. The optimal timing of delivery is critical, with chemotherapy being most effective when administered five days after CD40 treatment.
A study published in The Journal of Experimental Medicine found that hyper-aggressive immune cells that consume glucose may drive the development of coronary artery disease. Blocking this glucose overconsumption prevented inflammation and atherosclerosis, suggesting new therapeutic interventions to prevent heart attacks.
Macrophages produce excess inflammatory cytokine IL-1beta when damaged mitochondria release signals; p62 coats damaged mitochondria, ensuring removal. This prevents chronic inflammation and potentially age-related diseases.
Researchers found that certain bacteria, including Francisella tularensis and Salmonella enterica, can spread rapidly throughout the body by interacting with immune cells called macrophages. This process, known as trogocytosis, allows bacteria to evade detection and survive inside infected cells.
Researchers have successfully flipped macrophages from a pro-cancer, wound-repair promoting phenotype (M2) to an anti-tumor, kill-type (M1) phenotype. This breakthrough could lead to improved cancer immunotherapies by enhancing the body's natural killer cells' ability to target tumor tissue.
New research reveals that neurons in the gut play a crucial role in regulating inflammation and protecting intestinal tissue from over-reacting. The study, published in Cell, found that specific types of macrophages are activated by signals from neurons to prevent excessive inflammation.
Researchers discovered that human macrophages can divide and self-renew by activating a gene network similar to one found in embryonic stem cells. This finding could provide new directions in regenerative medicine and therapies, potentially replacing diseased tissue without using embryonic or induced pluripotent stem cells.
Researchers at Washington University School of Medicine suggest atherosclerosis is driven by processes similar to brain diseases like Alzheimer's and Parkinson's. Protein buildup inside macrophages, facilitated by p62, interferes with their ability to function.
A Drexel University biomedical engineer is exploring the potential of macrophages to grow blood vessels and promote wound healing through a natural process. The goal is to develop a drug delivery strategy that controls macrophage behavior and encourages vascularization by the body's own cells.
Researchers demonstrate CCL2 activates healing inflammatory immune responses and gene expression to promote nerve regeneration. Macrophages triggered by CCL2 increase regenerative capacity of dorsal root ganglia neurons.
Researchers identified quebecol, a molecule in maple syrup with anti-inflammatory properties, and its derivatives show promise as potential treatments for arthritis and other inflammatory diseases. The discovery could lead to a new class of anti-inflammatory agents with reduced side effects.
Researchers from University Health Network have found a specific cell type plays a key role in maintaining healthy arteries after inflammation. A group of tissue macrophages can self-replicate and help to heal the vessel after inflammation. This discovery could provide new treatment options for cardiovascular disease.
Researchers at Case Western Reserve University have developed a stem cell treatment that mediates an immune response to spinal cord injury, reducing tissue damage and preserving function. The treatment, involving multipotent adult progenitor cells (MAPCs), was effective in preventing the cascade of immune responses that often lead to l...
A Vanderbilt University Medical Center study found that COX-2 drugs may cause cardiovascular problems due to prostaglandin production by macrophages. The researchers hope to develop new, targeted painkillers without the vascular effects of existing medications.
Researchers discovered a mechanism where mesenchymal stem cells recruit and suppress macrophage activity to protect themselves from damage. This process allows macrophages to repurpose damaged mitochondria for their own survival, creating a mutually beneficial relationship between the two cell types.
Researchers discovered that macrophages and monocytes actively participate in multiple sclerosis progression, exacerbating disease severity through stress signals. The study highlights the significance of the crosstalk between the peripheral immune system and brain, opening new avenues for potential therapies.
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.