Scientists at Imperial College London discovered a way to reprogram macrophages, immune cells that cause inflammation, by blocking a single enzyme. By targeting this broken metabolism, they reduced inflammation in rats and mice with human-like diseases.
A new study reveals that particle-induced cell death depends on multiple redundant cathepsins, which can be blocked by inhibiting or silencing these enzymes in macrophages. The researchers found that several key proinflammatory events induced by sterile particles are blocked, including cell death.
A study published in the Journal of Clinical Investigation reveals a mechanism to reverse disease in arteries by targeting an immune reaction. Researchers at NYU Langone Health discovered that certain immune cells can switch from promoting inflammation to healing, which can lead to reduced plaque growth and improved cardiovascular health.
Macrophages from CAD patients suppress T cell activation, driven by pyruvate and PD-L1. This mechanism may contribute to immune dysfunction and reactivation of long-latent viruses like varicella zoster virus.
Research reveals a defective immune cell's sweet tooth predisposes people to shingles, exacerbating heart disease. The connection shows how the same mechanism disabling immune response to viral infections also affects heart conditions.
Macrophages, known as the Pac-Man of the immune system, promote healing by regrowing severed nerves in rats, offering a promising alternative to current treatments like autografts. The approach uses biological signals to recruit younger, undifferentiated cells destined to become pro-healing macrophages.
Trehalose boosts autophagy in macrophages, allowing them to reduce atherosclerotic plaque. The study shows promise for treating atherosclerosis and other metabolic conditions.
Researchers found that radiation therapy can improve the delivery of cancer nanomedicines up to 600% by attracting macrophages to tumor blood vessels, leading to increased nanoparticle uptake. This combination strategy shows promise for enhanced treatment efficacy and could be tested in clinical trials quickly.
Researchers at the University of Montreal Hospital Research Centre discovered a way to modify white blood cells to accelerate cutaneous healing. The treatment uses a special protein called MFG-E8 to control macrophage behavior, promoting anti-inflammatory and pro-reparatory reactions.
Researchers at the University of Kentucky discovered that macrophages play a crucial role in complex tissue regeneration in mammals. The team found that specific subtypes of macrophages are required for regeneration, which could lead to novel clinical approaches to restore damaged tissue in humans.
A compound called interleukin 4 helps macrophages kill parasites and promote healing in lung tissue by binding to a receptor called myosin 18A. This discovery could lead to better treatments for common infections, including those caused by parasitic worms that infect hundreds of millions of people worldwide.
Researchers discovered that tumor-associated macrophages steal checkpoint blockade antibodies from T cells, leading to improved responses in mouse models. Blocking FcγR receptors allows checkpoint inhibitors to effectively target cancer cells.
The KAIST team discovered a new molecular signal triggered by IPMK enzyme in mediating innate immune response to sepsis. This finding suggests a potential therapeutic target for treating serious medical conditions like neuroinflammation and polymicrobial sepsis.
Phagocytosis not only eliminates useless cells, but also 'educates' macrophages, the immune cells that carry it out. This process helps maintain tissues in a clean and healthy state. Researchers identified specific molecular toolkits for eliminating unwanted cells in each tissue.
Researchers created a new model to study how chlamydia interacts with the human immune system, identifying key players IRF5 and IL-10RA. The results suggest these genes could be drug targets for new treatments.
A recent study has discovered that macrophages are essential for the normal functioning of the heart, helping conduct electric signals that coordinate heartbeat. The findings suggest that changes in macrophage numbers or properties may contribute to heart rhythm abnormalities.
Researchers discovered that macrophages aggregate around cardiac cells to facilitate electrical conduction, helping the heart beat in rhythm. This finding suggests a new role for immune cells in electrophysiology and may lead to new therapeutics for heart disease.
Researchers at UNC School of Medicine have found that HIV persists in macrophage cells, a type of white blood cell, which has significant implications for HIV cure research. This discovery demonstrates that two types of cells may be targets for therapeutic intervention to eradicate the virus.
Researchers at NYU Langone Health have uncovered a critical pathway by which pancreatic cancer cells evade the immune system, involving high levels of two proteins - dectin-1 and galectin-9. The study found that blocking this interaction can increase survival in mice with pancreatic tumors.
Researchers found that inhibiting Toll-like receptor 4 activation can silence Ebola virus-infected macrophages, a potential treatment option. The study also suggests this approach could work for other hemorrhagic fever viruses.
Scientists discovered that obesity disrupts the balance of 'guardian immune cells,' which maintain a delicate balance between immune systems. In healthy states, these cells protect against inflammation and metabolic disease, but in obese individuals, they lose their regulatory function.
Researchers discovered that macrophages transmit messages between non-immune cells, such as pigment cells in fish, to facilitate complex patterns like stripes. This unique function of macrophages suggests they may play a broader role in intercellular communication, affecting tissue development, regeneration, and cancer.
Researchers found a previously unappreciated role for Abraxane in tumor immunology, suggesting ways to improve the drug and develop new combination treatments. Nab-paclitaxel enables macrophages to switch from immune-suppressing M2 cells back into M1 cells that amplify the body's effort to kill cancer cells.
Researchers develop 'release and kill' strategy to target M. tuberculosis in infected macrophages, potentially shortening TB treatment periods. The approach leverages selective apoptosis to release the bacteria from infected cells, making them susceptible to antibiotics.
A research group at Kobe University has discovered a potential new cancer treatment that activates cancer-engulfing cells. The treatment uses an antibody to activate macrophages, which can effectively eliminate cancer cells. This discovery could lead to the development of new and more effective cancer treatments.
Researchers from Geneva and Fribourg have developed a rapid screening method to select the most promising nanoparticles for medical applications. The new approach can determine biocompatibility in under two days, reducing the need for animal testing and enabling personalized treatment.
Researchers identified how HIV infects macrophages despite protective protein SAMHD1 being switched off. A treatment to maintain macrophage defences could be crucial for reaching an HIV cure.
ABX464 upregulates IL-22 and miR-124, showing strong anti-inflammatory effects in preclinical models. The compound also prevents intestinal inflammation and protects against colitis, with therapeutic effects lasting at least 6 weeks.
Johns Hopkins researchers have identified a critical cellular switch that turns on the inflammatory immune response contributing to asthma attacks. By inhibiting this pathway, they may be able to prevent continued inflammation and long-term structural changes in the lungs.
A recent study suggests that high-density lipoprotein (HDL) cholesterol may not always protect against heart disease as previously thought. HDL can actually enhance the inflammatory response of immune cells called macrophages, which counteracts its established anti-inflammatory effect in other cell types.
A recent study published in JCI Journals reveals that immune cells, specifically perivascular macrophages, play a crucial role in the development of dementia in individuals with hypertension. The research suggests that targeting these cells may be a potential approach for preventing cognitive decline in high blood pressure patients.
A study by TSRI researchers reveals that macrophages can create vessel-like structures for delivering oxygen and nutrients to growing tumors, promoting cancer progression. This finding could lead to novel cancer therapies targeting immune system cells.
A team of researchers at UC San Diego School of Medicine successfully reversed diabetic insulin resistance and glucose intolerance in mouse models by removing the protein galectin-3 (Gal3). This finding suggests that Gal3 inhibition could be an effective way to treat type 2 diabetes.
La Jolla Institute for Immunology researchers have developed a new method to inactivate specific genes in immune cells using enhancer targeting. This approach allows for the precise deletion of genes in one cell type while leaving others intact, opening up new possibilities for targeted therapies.
Scientists discover that heme molecule interferes with macrophage cytoskeleton, immobilizing them and preventing immune cells from eliminating bacteria. Quinine, an existing malaria medication, restores functionality of affected macrophages, paving the way for new treatment possibilities.
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.
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.
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.
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.
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.
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 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.