Articles tagged with Macrophages
A study reveals that smooth muscle cells near necrotic cores of atherosclerotic plaques produce complement protein C3, stimulating macrophage activation and driving clonal expansion. The cells' ability to evade immune surveillance is restored by inhibiting CD47, suggesting these cells as viable therapeutic targets.
Researchers discovered that M2-type macrophages are more susceptible to ferroptosis and may exacerbate chronic inflammation. A mathematical model was developed to describe the stability of macrophages under different conditions.
Researchers at the University at Buffalo have discovered that hematopoietic stem cell transplantation improves Krabbe disease outcomes through a mechanism independent of cross-correction. The study found that macrophages expressing GALC enzyme aid in myelin debris degradation, leading to better patient outcomes.
Researchers at University of Nottingham have developed biomaterials that can control the body's immune response, potentially reducing implant rejection rates. The new materials use surface shape and chemical composition to influence macrophage attachment and behavior.
Researchers at Harvard's Wyss Institute have created disc-shaped particles that control macrophage behavior to slow tumor growth and metastasis in mice. The 'backpacks' keep macrophages in their tumor-killing state for up to five days, reducing the size of tumors and metastatic nodules.
Researchers have found that elevated ferritin concentrations are associated with increased production of special signalling molecules, leading to complications and death in COVID-19 patients. Marker CD163 is also an important indicator of macrophage activation and high risk of complications.
A new study at CNIC discovers a molecular mechanism regulating macrophages, key immune sentinels. The research may lead to cancer treatments and tissue repair by targeting these cells.
Researchers develop new type of immunotherapy targeting macrophages in omental fat, which appears to reduce ovarian cancer spread and tumour growth. The study shows promise for improving treatment outcomes, but further testing is needed.
Researchers identified 497 genes expressed in resistant mice and 22 genes in susceptible mice, showing the development of disease depends on host genetics. The study aims to develop biomarkers for diagnosis and treatment of leishmaniasis.
Scientists have successfully engineered CAR macrophages to target and kill solid tumors, using a novel approach that could lead to more effective cancer treatments. The discovery centers around harnessing the immune-boosting properties of macrophages, which are often co-opted by tumors.
Researchers have found a new mechanism for long-lasting pain relief through the production of endogenous opioids by immune cells. The discovery uses cytokine interleukin-4 to induce M2 macrophages, which produce opioids and reduce pain, offering potential alternative pain management options.
Research suggests that beta cells produce signals that aid their own demise in Type 1 diabetes, leading to increased inflammation and damage. The study found that the absence of a specific enzyme enhances anti-inflammatory responses, while its overexpression promotes inflammatory ones.
Researchers discovered that shortly after a stroke, macrophages from the blood attack dead and adjacent healthy brain tissue. This process was hindered by inactivating the Cxcr4 gene, which acts like an antenna for inflammatory processes in the brain.
Researchers have discovered that heterotopic ossification, a painful complication of trauma, is caused by macrophages sending errant signals to bone-forming stem cells. A new study suggests that targeting TGF-beta expressing macrophages may prevent this abnormal bone formation
A new biochemical switch involved in M2 macrophage polarization and proliferation has been identified, which can be targeted to inhibit cancer growth. The discovery was made by a research team from the University of Vienna and could lead to novel therapies against systemic diseases and cancer.
Scientists at DESY used an advanced X-ray combination technique to trace nanocarriers for tuberculosis drugs within cells with high precision. The method also revealed the calcium content in human bone, benefiting osteoporosis research.
Researchers at Columbia University Irving Medical Center found putrescine, a compound responsible for the foul smell of decomposing flesh, may help treat atherosclerosis. The study suggests putrescine's role in removing dead cells through efferocytosis could improve plaques and prevent chronic inflammation.
Researchers found that microglia, immune cells in the brain and central nervous system, encase macrophages, preventing them from dispersing into areas they shouldn't be. This discovery may lead to new treatments for conditions like multiple sclerosis and Alzheimer's disease.
Researchers at University of Oxford have identified a new target for repairing the heart after a heart attack by modulating the immune response. Macrophages play a key role in forming cardiac scars, and modifying their behavior could lead to more efficient repair and potentially avoid heart failure.
Researchers at Tokyo University of Science discovered a novel anti-cancer strategy targeting tumor-associated macrophages (TAMs) by regulating FROUNT protein. Disulfiram, an alcoholism treatment, was found to inhibit cancer cell growth and suppress TAM movement in animal experiments.
Researchers have invented a Trojan Horse nanoparticle that selectively targets and eats away at plaque-causing cells, reducing plaque size and stabilizing it. This approach shows promise as a potential treatment for atherosclerosis, the leading cause of death in the US.
Toxoplasma gondii injects proteins into host macrophages, altering their behavior and suppressing the immune response. This manipulation leads to the creation of M2 macrophages, which reduce inflammation and allow the parasite to evade elimination by T cells.
Researchers have discovered a rare African-specific variant of the TP53 gene that causes iron accumulation in macrophages, leading to poorer responses to bacterial infections. However, this variant also improves response to malaria toxin, potentially offering protection against severe inflammation and disease severity.
A new study reveals that high-protein diets can lead to increased plaque buildup in arteries, particularly unstable plaque prone to rupture. This can increase the risk of heart attacks. Researchers found that excess amino acids from a high-protein diet activate macrophages, leading to cell death and worsening plaque complexity.
A recent study published in PNAS reveals that extracellular matrix protein-1 (ECM1) plays a crucial role in the pathogenesis of ulcerative colitis, a type of inflammatory bowel disease. The researchers found that ECM1 is highly expressed in macrophages and regulates their polarization through the GM-CSF/STAT5 signaling pathway.
Researchers study how gut infections damage the nervous system, leading to chronic inflammation and conditions like IBS. They find that specific genes contribute to cell death and propose potential treatments by boosting polyamine production or restoring gut microbial communities.
Researchers have found that deleting the BMAL1 clock gene makes immune cells more effective at fighting off pneumonia-causing bacteria. The study reveals that strengthening the actin skeleton of these cells is key to their increased effectiveness.
Scientists at Ohio State University have created a treatment for late-stage sepsis using nanotechnology to transform donated immune cells into a powerful antibacterial drug. The therapy demonstrated significant improvements in survival rates and bacteria clearance in mouse models of sepsis.
Macrophages change their metabolism drastically after coming into contact with bacteria, triggering an inflammatory response. This process involves the activation of Toll-like receptors, which leads to histone acetylation and changes in gene expression.
Researchers discovered that Crohn's disease-associated bacteria can switch between replicating and non-growing states within macrophages to tolerate antibiotics. This stress response allows a reservoir of antibiotic-tolerant bacteria to survive in the host and cause long-term inflammation and irritation.
A study suggests that monocyte-derived macrophages can induce lung fibrosis without prior alveolar epithelial cell injury. The research found increased flux through the mevalonate pathway in bronchoalveolar cells from IPF patients, which exacerbates fibrosis.
A new method has been developed to identify aggressive breast cancer by analyzing tumor tissue signatures, showing a correlation with poor outcome in patients. The study used mouse models and bioinformatics expert to isolate macrophages from mice affected by breast cancer and compared them with those from healthy breast tissue.
A new study by University of Chicago researchers reveals how lactate regulates immune cell function and contributes to cancer growth. The discovery offers a potential breakthrough in developing targeted therapies for various types of cancer.
The study reveals that the GAS7 protein's BAR domain is essential for phagocytic cup formation, enabling macrophages to efficiently consume debris. The protein's oligomerization and membrane binding are critical for this process.
Researchers at Texas Biomedical Institute are studying lung macrophages and their role in TB infection, with the goal of developing a new set of biological pathways critical to the body's response. The findings could lead to a new strategy for host-directed therapy and potentially cure TB.
Researchers at University of Utah Health identified large immune cells containing oily droplets in the lungs of vaping patients, enabling faster diagnoses and shedding light on the mysterious condition. The discovery may lead to better treatment options and a deeper understanding of the illness's causes.
Researchers discovered two distinct sub-populations of interstitial macrophages in the lung, which play a crucial role in preventing asthma development. These sub-populations exhibit different functions, origins, and morphologies, and have distinct local precursors.
Researchers have discovered a new form of immunotherapy that targets and removes specific immune cells called macrophages, which support cancer growth. The technique has shown promising results in treating malignant melanoma, with tumors shrinking after the removal of these cells.
Researchers found large diversity in neutrophil and macrophage frequencies, with some tumors attracting one type while others attract the other. The study highlights heterogeneity of tumor cells and immune microenvironment as important considerations for therapy.
Researchers at UC San Diego have developed a new therapeutic approach to convert tumor-associated macrophages (TAMs) into cancer killers. The antibody, LM609, induces ADCC and kills drug-resistant tumors, prolonging response to standard treatments.
Researchers at Johns Hopkins Medicine developed a new mouse model that mimics the effects of red blood cell transfusions on human infants with necrotizing enterocolitis (NEC). The study found that severe anemia increases the risk of NEC after transfusion, and that free hemoglobin can trigger an immune response in the intestine.
Researchers found that whole body vibration increases levels of Alistipes, a bacterium producing short chain fatty acids that decrease inflammation. This shift also improves the balance between macrophages promoting and suppressing inflammation.
Researchers at Stanford University School of Medicine have discovered a new 'don't eat me' signal used by cancer cells to evade immune detection. Blocking this signal allows immune cells to attack and destroy cancer cells in mice implanted with human cancers, providing a potential basis for new anti-cancer therapies.
Researchers have identified a molecule called Gas6 that induces macrophages to clean up cellular debris and reduce inflammation. Boosting Gas6 levels in macrophages has been shown to resolve inflammation in mouse models of acute lung injury, holding promise for treating diseases such as heart disease, cancer, and rheumatoid arthritis.
Researchers at Johns Hopkins Medicine discovered that certain forms of heart disease may result when circulating anti-inflammatory white blood cells fail to properly differentiate into macrophages. Blocking a key protein, IL-17A, permits healthy cardiac function and allows macrophages to protect the heart muscle.
A new study identifies an enzyme critical for normal wound healing in diabetes, suggesting a potential treatment with allopurinol. In diabetic mice, blocking uric acid production improved healing rates.
Research found that extracellular vesicles derived from kids' fat can disrupt cholesterol disposal in various tissues, regardless of weight. The study suggests that fat tissue plays a pivotal role in triggering cardiovascular disease, even before symptoms appear.
Researchers uncover the role of macrophages in causing pelvic pain in endometriosis, potentially leading to new non-hormonal treatments. The discovery was published in The FASEB Journal and found increased production of IGF-1 by macrophages, which encourages nerve growth and activation.
Scientists deciphered how YopO changes its shape to confuse the immune system, disrupting communication and allowing bacteria to evade digestion. Understanding this process may lead to developing targeted, tailor-made substances to inhibit plague pathogens.
In the absence of gasdermin D, caspase-1 induces apoptosis, but not pyroptosis, in macrophages. Caspase family members caspase-3 and caspase-9 are involved in this process. The study suggests that caspase-1 activates Bid, a pro-apoptotic protein, which induces cytochrome c release from mitochondria and subsequent apoptosis.
Researchers used advanced imaging techniques to visualize macrophages in living mice with brain tumors, finding clear morphological and behavioral differences between blood-derived and brain-resident macrophages. Blocking macrophage infiltration improved survival in treated mice.
Scientists at the University of Illinois found that three phenolic compounds in cocoa bean shells can repair damaged mitochondria, block inflammation, and restore insulin sensitivity in white fat cells. The study suggests that consuming these compounds could prevent mitochondrial dysfunction in adipose tissue.
Researchers found that extracellular pathogens like Pseudomonas aeruginosa can enter host cells and induce cell lysis through the type III secretion system. The study reveals a new mechanism of bacterial killing in macrophages.
Scientists have made a breakthrough in understanding how macrophage cells respond to certain bacteria, potentially leading to new treatments for Crohn's Disease. The study found that different types of macrophages exhibit distinct molecular mechanisms when switching off their pro-inflammatory behavior.
Research at MD Anderson Cancer Center discovers a symbiotic circuit between PTEN-deficient glioblastoma cells and macrophages, which creates a mutually supportive relationship. Inhibiting LOX, a novel attractor of macrophages, shrinks tumors and blocks macrophage infiltration.
Under hypoxic conditions, fewer metabolites are produced in the citric acid cycle, reducing bacterial reproduction in macrophages. This discovery provides a new method for pathogen control that doesn't rely on oxygen levels.
Researchers at Virginia Tech have gained a new understanding of the complex interactions between macrophages and fibroblasts as they work together to clean up and repair damaged tissue. The study shows that manipulating the environment around these cells could lead to improved treatments for wounds and tumors.
Researchers identified a new molecular mechanism causing rheumatoid arthritis, finding that death of macrophages triggers the disease. The protein A20 was found to prevent macrophage death and protect against arthritis.
A new study uncovers the presence of 'hidden' microglia in the brain, which show a resemblance to microglia associated with Alzheimer's disease. The researchers hope to find strategies for controlling these immune cells to develop future treatments for neurodegenerative diseases.
Researchers have discovered a potential new treatment for renal fibrosis by selectively activating AT1 receptors on T cells, which may help limit scar formation in the kidney. The study found that activating these receptors mitigates renal fibrogenesis by inhibiting Th1 differentiation and renal accumulation of pro-fibrotic macrophages.