Articles tagged with Macrophages
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Researchers have identified a protein called CCL5 that protects macrophages from premature death during respiratory viral infections, allowing them to continue fighting the infection. This discovery may lead to new methods to hasten recovery and reduce symptoms of influenza and the common cold.
Scientists have found tunneling nanotubules that enable immune cells to relay molecular messages, allowing them to coordinate responses to pathogens. The discovery could reveal new insights into the local inflammatory response and potential therapeutic strategies.
A study found that HIV-infected macrophages travel to the temporal lobe, causing inflammation and damaging memories. Researchers hope to develop drugs targeting these cells to prevent HIV-associated dementia.
Researchers identify how nuclear receptors work to suppress inflammatory responses, potentially leading to more powerful anti-inflammatory drugs with fewer side effects. This discovery could lead to better therapeutic results in treating diseases such as arthritis and arteriosclerosis.
Scientists discover a new connection between macrophages and lymph vessels in the eyes, which could lead to new therapies for eye diseases like diabetic retinopathy. The study also suggests that this link may be universal and involved in spreading cancer.
Researchers have discovered a novel Group B Streptococcus (GBS) gene, iagA, that helps the bacteria invade the human blood-brain barrier, leading to meningitis. A glycolipid treatment has been found to induce long-term anergy in natural killer T cells, which could impact its use as an immune activator.
Researchers discovered that CD11b-positive macrophages play a crucial role in the development of lymphangiogenesis in the cornea during inflammatory conditions. These macrophages transform into endothelial cells or stimulate the division of existing lymphatic cells, leading to the formation of new lymph vessels.
Certain bacteria, such as Rhodococcus equi, have evolved strategies to survive and even multiply within macrophages, which are intended to digest pathogens. This occurs when the bacteria prevent phagosome development, avoiding acidification and lysosomal digestive enzymes.
A new device has been developed to detect inflammatory cells in blood vessels, which are associated with critical atherosclerotic plaques. The device uses fluorescence spectroscopy to identify macrophage infiltration in the fibrous cap, a key marker of plaque inflammation.
Researchers find biglycan acts as endogenous ligand of Toll-like receptor 4 in macrophages, increasing responses and leading to improved survival in sepsis. Mice lacking biglycan show increased survival benefit, highlighting the protein's pro-inflammatory role.
A study by University of Illinois-Chicago researchers found that a plasminogen system component called PAI-1 actually enhances muscle regeneration when deficient. This suggests the plasminogen system may have multiple roles in muscle repair and offers potential therapeutic targets for aging and degenerative diseases.
Research reveals how a molecule helps Brucella bacteria evade destruction within macrophages, leading to a deeper understanding of the pathogen. This discovery has significant implications for developing new vaccines and treatments against Brucellosis.
A recent study published in Cell Metabolism discovered a novel link between a molecule called apoptosis inhibitor of macrophage (AIM) and the development of atherosclerosis. AIM, which typically protects infection-fighting cells, was found to promote plaque buildup inside arteries when its function is suppressed.
A study found that air pollution increases the risk of heart attacks and strokes by thickening blood, a process triggered by particulate matter. Exposure to pollutants boosted inflammatory activity and promoted clotting factors in cells, suggesting a potential link between air pollution and cardiovascular disease.
Researchers found that deleting pro-inflammatory enzyme IkB kinase â (Ikk-â) from immune cells' macrophages improves insulin sensitivity, offering hope for new type II diabetes treatments. The study suggests targeting myeloid cells and their macrophages as a potential strategy for treating the disease.
The study reveals that Rb plays a crucial role in regulating cell proliferation and apoptosis, two key processes affected in cancer development. By analyzing mice lacking Rb during embryonic development, researchers found that red blood cells failed to mature, highlighting the importance of Rb in maintaining normal cellular function.
Researchers identified a novel oncogene in Chernobyl residents with papillary thyroid cancer, resulting from the fusion of the AKAP9 and BRAF genes. This study provides evidence that chromosomal inversions are a common molecular lesion in post-Chernobyl thyroid cancers.
A new drug, GW7647, demonstrates profound protective effects against atherosclerosis by reducing lipid accumulation in macrophages. The study highlights the potential of targeting multiple PPARs, particularly PPARalpha and PPARgamma, to limit lipid accumulation and reverse atherosclerosis.
A new study links resistin to inflammation, insulin resistance, and obesity. Resistin levels increase in human macrophages treated with endotoxin or cytokines, suggesting a role in promoting diabetes through insulin resistance.
Researchers find that blocking annexin 2 or eliminating it from cell surfaces can prevent HIV infection in macrophages. Annexin 2 helps the virus deliver its genetic material into cells by binding to a surface component on the virus.
Vascular tumor growth in children is linked to a protein called MCP-1 that recruits macrophages, stimulating angiogenesis and tumor growth. Anti-MCP-1 therapy may prevent tumor development and improve patient outcomes.
Researchers at OHSU's Oregon Stem Cell Center have discovered that macrophages, not stem cells, can fuse with diseased liver cells to correct genetic liver disease in mice. This finding suggests that transplantation of macrophages alone may be a more targeted and effective treatment approach than traditional stem cell therapy.
A study published by Temple University researchers debunks the longstanding 'Trojan Horse' model of HIV-caused dementia. They found that a large, late invasion of HIV-infected macrophages into the brain is responsible for the disease, not early latent infection as previously thought.
A Temple virologist has received a grant to investigate the role of macrophages in HIV dementia complex. The researcher aims to understand how these cells contribute to the development of the condition, which affects 10% of AIDS patients, and explore potential therapies to target them.
Researchers discovered reduced lysozyme levels in HIV-demented patients' macrophages, suggesting impaired immune function and increased vulnerability to infections. The finding could lead to a marker for monitoring disease progression and potential new treatment targets.
Researchers at Jefferson Medical College have found that the HIV virus produces proteins that trigger biochemical pathways in the brain, resulting in brain cell death and dementia. The study suggests that removing the virus or its associated proteins may be an effective way to prevent or treat HIV-related dementia.
Researchers at UT Southwestern Medical Center have found evidence of a substance secreted by the lungs of a developing fetus that contains the key signal to initiate labor. The study, led by Dr. Carole Mendelson, suggests a link between a specific fetal lung protein and labor in humans.
UCSD School of Medicine researchers have identified a mechanism leading to life-threatening infections, where PKR protein causes macrophages to die, allowing bacteria to spread. The discovery may help develop inhibitors for PKR, controlling nasty infections and reducing flu-related deaths.
A study found that women who experienced miscarriage had lower concentrations of macrophage inhibitory cytokine-1 compared to those who delivered normally. Low MIC1 levels often preceded miscarriage, suggesting its potential as a predictor and therapeutic target for pregnancy loss prevention.
Researchers at UCSD have identified a protein molecule targeted by anthrax toxin that prevents cytokine production, allowing bacteria to evade the immune system. By understanding this mechanism, scientists may develop new drugs to protect against anthrax infections.
Two studies found that macrophage infiltration of adipose tissue is characteristic of human obesity and precedes insulin resistance. Treatment with an insulin-sensitizing drug triggered downregulation of inflammatory genes, suggesting a potential therapeutic target.
A study on beclin 1 autophagy gene reveals its role in tumor suppression. In another study, researchers found that obese fatty tissue is characterized by inflammation, which may contribute to insulin resistance. These findings suggest that autophagy and inflammation play crucial roles in cancer biology and obesity-related diseases.
A new study shows that moderate exercise reduces susceptibility to upper respiratory tract infection by enhancing immune function. Soluble oat fiber â-glucan also boosts immunity, and combining it with exercise may have additional benefits.
NF-kappaB plays a complex role in atherosclerosis, both promoting and inhibiting inflammation. In mice deficient in LDL receptors and NF-kappaB activation, lesions were larger and more advanced, containing more necrosis and macrophages.
Researchers have found a way to extend the lives of chilled platelets after transfusion, potentially increasing the platelet supply and making it easier to transport. This breakthrough could help more patients receive life-saving platelet transfusions.
Researchers at Scripps Research Institute identify a single protein called Trif that associates with different receptors to detect pathogens, triggering immune reactions. The protein could be a potential target for intervening in diseases like sepsis.
Researchers show that SOCS3 slows macrophage activation initiated by IL-6, and discover an unexpected pathway causing fatal inflammatory responses in humans., The study adds to understanding of the JAK/STAT signaling pathway in immune system cells.
Researchers found that fully differentiated blood cells retain their ability to switch identity, challenging the long-held idea of fixed cell types. The discovery has potential applications in replacing damaged cells in blood diseases and neurodegenerative disorders.
A UCSF study found that macrophages from human lymphoma patients can cause mouse lymphoma when injected into mice. This contradicts the current understanding of macrophages' role in fighting disease. The researchers believe HIV-infected macrophages can become neoplastic and stimulate lymphoma growth.
A research team led by Wake Forest and Johns Hopkins universities found that mutations in the MSR1 gene are associated with an increased risk of aggressive prostate cancer, particularly in African-American men. The study identified seven potentially important mutations of the MSR1 gene, including one that leads to rapid metastasis.
Researchers found that blocking interleukin-1 can prevent additional brain tissue damage, suggesting a new potential treatment for traumatic brain injury and neurodegenerative diseases. By inhibiting IL-1, macrophage activation is reduced, leading to less inflammation and cell death.
Researchers at MGH identified a key immune system molecule, PGRP-LC, essential for recognizing and ingesting gram-negative bacteria like E.coli. The protein plays a crucial role in the macrophage's response to infection.
Researchers used DNA arrays to understand macrophage responses, revealing that specific bacterial components can activate the immune system. This knowledge will help design therapeutics with fewer side effects and improve disease treatment.
The amyloid beta protein found in plaques stimulates the production of toxic substances that attract new surrounding cells, causing brain cell death. Astrocytes, normally involved in maintaining brain structure, slow down these processes and protect against inflammation.
New research suggests that macrophages are an underappreciated reservoir of virus in HIV infection. Macrophages continue to produce large amounts of an HIV-like virus even after CD4+ T cells are depleted, providing new insight on how the virus survives. This discovery may lead to new strategies for eliminating the virus from the body.
Researchers discovered an enzyme called isocitrate lyase (ICL) that allows TB bacteria to persist in macrophages and evade immune attack. A drug targeting ICL may reduce treatment time for chronic infection. The enzyme's crystal structure has been determined, providing clues for designing drugs to attack persistent TB bacteria.
Researchers found that macrophages can recognize foreign cells using the CD47 protein, not MHC class I as previously thought. This discovery challenges an important dogma and has implications for autoimmune diseases and ovarian cancer.
Investigations reveal that matrix metalloproteinases (MMPs) play a crucial role in communication between disc cells and macrophages, facilitating resorption. The discovery may lead to injectable therapies that encourage natural macrophage activity, offering a non-surgical alternative for herniated discs.
Scientists found that apoptosis induces the processing of EMAP II precursor protein, releasing a biologically active form that recruits macrophages. This process is crucial for tissue remodelling and coordinating cell death during embryonic development.
Macrophages may proliferate in response to HIV integration, causing disease through sequential pathogenesis. Researchers identify potential DNA-interacting drugs to treat AIDS dementia.
Researchers identified a molecular link that enhances cell-mediated antiviral response, which is critical for suppressing HIV replication. The CD86 molecule on macrophages plays a key role in this response, and blocking its interaction with CD8+ cells reduces the immune system's ability to fight the virus.
Scientists at Wake Forest University Baptist Medical Center have found a way to inactivate the CCR5 co-receptor, a doorway for early-stage HIV-1 virus, on the surface of macrophages and lymphocytes. This approach could be used to treat early-stage HIV-infected individuals and potentially prevent infection.
Researchers at Washington University School of Medicine discovered that E. coli can live inside immune-system cells lining the bladder wall, making it harder to treat bladder infections. The bacteria use sticky appendages to cling to these cells and evade antibiotics.
A new study reveals that tissue macrophages play a critical role in triggering the production of HIV in patients with AIDS, leading to increased virus levels despite declining CD4 T cell counts. This finding highlights the importance of controlling opportunistic infections to slow the cycle of virus production.
A study by Prof. Michal Schwartz explains why mammals can't regenerate damaged central nervous system tissue, offering hope for treatment development. Researchers found that macrophages play a crucial role in wound-healing, and 'educating' them may help overcome this obstacle.