Sentences with phrase «infection by immune cells»

Not exact matches

Autoimmunity is commonly caused by bacterial infections or overgrowth in the small intestine, in which partially digested food compounds are incorporated into bacterial cell walls and then the immune system, reacting to the bacteria, forms antibodies that also recognize food compounds, some of which might cross-react with human counterparts.

When viral and bacterial infections strike, our bodies respond by commanding B cells within our immune systems to crank out antibodies to battle the invaders.

And a new analysis of the STEP trial, published last November in Proceedings of the National Academy of Sciences USA, provides a warning that the very vectors (adenoviruses, which are also employed in other vaccine development work) used to distribute the inactive HIV strains can actually make the immune system more vulnerable to infection by recruiting susceptible T cells to mucous membranes, where they are more likely to be infected during sexual activity.

Chronic HIV infection results in exhaustion of the immune system, a phenomenon characterized by dysfunctional HIV - specific killer T cells.

They demonstrated that PS extracts protect blood and immune cells from infection by HIV - 1, the most widespread type of HIV.

«Our immune system is made up of specialised cells that move through blood and tissue, preventing disease and fighting infection by distinguishing between what is the body's own healthy tissue and what is foreign.

Encased in bone and protected by a special layer of cells, it is shielded from infections and injuries — but also from many pharmaceuticals and even from the body's own immune defenses.

Outside of the brain, cytokines are released by immune cells fighting infections, and they can alter MHCI expression in a complicated feedback loop.

By studying infected cells grown in a laboratory, the team found that a large number of CMV's genes help it hide from the immune system by allowing it to destroy many of the proteins produced by the body during virus infection and preventing them from activating immune cells to destroy the viruBy studying infected cells grown in a laboratory, the team found that a large number of CMV's genes help it hide from the immune system by allowing it to destroy many of the proteins produced by the body during virus infection and preventing them from activating immune cells to destroy the viruby allowing it to destroy many of the proteins produced by the body during virus infection and preventing them from activating immune cells to destroy the viruby the body during virus infection and preventing them from activating immune cells to destroy the virus.

In particular, it has evolved to show itself three to nine months after infection, allowing its own destruction by displaying antigens on its cell surfaces so the dog's immune system can destroy it.

Interferons are molecules produced by cells in response to viral or bacterial infection, and which act on neighboring cells to prevent the spread of the infection, shut down protein synthesis, and activate the immune system.

Patients can succumb to bacterial infections because their immune systems lack a molecule required by immune cells, specifically neutrophils, to go to the site of infection.

The reason for the reduced glucose levels associated with bacterial meningitis was believed to be the need for glucose as fuel by infiltrating immune cells in response to infection.

«We found that expression of glucose transporters is completely shut down by bacteria, leaving insufficient fuel for the immune cells to fight off the infection,» said the study's first author, Subramanian Krishnan, PhD, of the Division of Infectious Diseases at CHLA.

T cells help protect the body from parasites by traveling to the site of infection and recruiting other immune cells to mount an attack.

Cells in the innate immune system respond immediately by secreting inflammatory factors called cytokines to stop the spread of infection.

S. mansoni IPSE binds to Immunoglobulin E (IgE), an antibody produced by the immune system that is expressed on the surface of basophils, a type of immune cell; and mast cells, another immune cell that mediates inflammation; and sequesters chemokines, signaling proteins that alert white cells to infection sites.

When challenged by a toxin or infection, the immune system screens this population for a match, then swiftly multiplies the clonal cell line that produces the matching antibody.

In a study led by Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research member Dr. Julian Martinez - Agosto, UCLA scientists have shown that two genes not previously known to be involved with the immune system play a crucial role in how progenitor stem cells are activated to fight infection.

The analysis performed revealed that many variations in immune cell function triggered by chronic HIV infection are associated with high levels of bNAbs.

The gene codes for an immune receptor on red blood cells; lack of that receptor prevents infection by Plasmodium vivax, a species of the malaria parasite.

«Our study shows a whole new route, or bypass mechanism, for triggering the body's adaptive immune response to TB infection, a means by which infected dendritic cells cooperate with uninfected dendritic cells to activate T cells and respond to the infection,» says infectious disease specialist and study senior investigator Joel Ernst, MD, a professor at NYU Langone Medical Center.

Some have proposed that age - associated inflammation is caused by accumulating wear and tear on our immune cells, while others have suggested that it is caused by immune cells dealing with chronic viral infections.

«This debris left by dead cells can mistakenly signal to the body that there is an infection that warrants immune action, triggering the innate immune system,» said Bruce A. Sullenger, Ph.D., director of the Duke Translational Research Institute.

They lie dormant and can not be eliminated by anti-retroviral therapy, nor by the weakened immune system, so that if treatment is stopped at any time, the virus starts to replicate and infect more cells again, while the immune system can not suppress this rebound of HIV infection.

Research led by scientists at the Gladstone Institutes has identified the precise chain of molecular events in the human body that drives the death of most of the immune system's CD4 T cells as an HIV infection leads to AIDS.

They found that these skin - resident immune cells function as «first responders» to skin injuries in part by producing the molecule known as interleukin - 17A (IL - 17A), which wards off infection and promotes wound healing.

The infection rapidly turned on a wide range of genes involved in immune system activation and cell death, they conclude, bolstering the hypothesis that the greatest harm may not have been done by the virus itself, but by an over-reactive immune system.

In most cases, infected epithelial cells are quickly killed by CD8 + cells, a type of white blood cells; only occasionally does the infection overwhelm the immune system, resulting in a lesion.

Building on that work, the current paper looked at a less lethal strain, the H1N1 «swine flu,» that does not infect neurons, but which, the researchers showed, still caused inflammation in the brain via inflammatory chemicals or cytokines released by immune cells involved in fighting the infection.

They used the gene - editing CRISPR / Cas9 technique to sift the genomes of melanoma cells for changes that made tumors resistant to being killed by immune T cells, which are the main actors in the immune system response against infections and cancer cells.

Retinal cell death can be induced by phagocytic immune cells that infiltrate the tissue in response to injury or infection, but the molecular signals that trigger phagocyte invasion are largely unknown.

Earlier research by Rafi Ahmed of Emory University found that such viral infections in mice stall the innate immune response by flicking on the PD - 1 switch, which keeps the T cells from functioning.

The studies, conducted separately on the East and West coasts of the United States, attempt to make the immune system resistant to HIV by crippling a receptor, known as CCR5, on T cells that the virus uses during the infection process.

Shortly after infection, HIV levels skyrocket, but then the immune system and other antiviral factors produced by cells drive down the amount of virus in the blood — the so - called viral load — and establish a «set point.»

As part of the body's normal, healthy immune response to infection, the barrier formed by blood vessel cells temporarily loosens, allowing white blood cells to exit the bloodstream and attack the invading bacteria or virus, Rehman said.

he body responds to tuberculosis infection by locking the bacterial offenders into tiny clusters of immune cells called granulomas, which are a hallmark of the disease.

One way they do this is by transporting the virus to the body's immune cells, without themselves becoming infected, through a process called trans - infection.

Taking advantage of infected patients, proprietary animal models of infection and new technological advances in the field of static and dynamic imaging, Immunopathology Unit tackles unresolved issues that include the means by which innate and adaptive immune cells traffic and function within the normal, cirrhotic or cancerous livers.

They did this not only by trans - infection, but also by making the immune cells more prone to infection by HIV.

Researchers have illuminated a crucial step in the immune system's response to infection by using live cell imaging to follow the movement of immune system cells that have been genetically...

Anna Huttenlocher, University of Wisconsin, USA Neutrophils in the Tumor Microenvironment Neutrophils, Wounds, and Cancer Progression Stefan Kaufmann, Max Planck Institute, Germany Pathology and immune reactivity: understanding multidimensionality in pulmonary tuberculosis Constitutive BAK activation as a determinant of drug sensitivity in malignant lymphohematopoietic cells Kathryn Moore, New York University, USA MicroRNA -33-dependent regulation of macrophage metabolism directs immune cell polarization in atherosclerosis Lalita Ramakrishnan, University of Cambridge, UK Myeloid Growth Factors Promote Resistance to Mycobacterial Infection by Curtailing Granuloma Necrosis through Macrophage Replenishment Beth Stevens, Harvard University, USA Microglia: Dynamic Mediators of Synapse Development and Plasticity Do glia drive synaptic and cognitive impairment in disease?

The awards span the broad mission of the NIH and include groundbreaking research, such as engineering immune cells producing drugs at the site of diseased tissue; developing a sensor to rapidly detect antibiotic resistance of a bacterial infection; understanding how certain parasites evade host detection by continually changing their surface proteins; and developing implants that run off the electricity generated from the motion of a beating the heart.

In a typical immune response, for instance, inflammatory proteins called cytokines will be released by immune cells at a site of inflammation and then other immune cells will use these cytokines like a trail of breadcrumbs to home in on the site of infection and destroy the pathogens that are causing it.

One avenue of our translational research aims to determine the impact of in utero HIV - 1 exposure on infant immunity to vaccinations and co-infections by dissecting the infant immune repertoire present at birth in the context of maternal HIV - 1 infection and how the infant T cell repertoire changes following early life exposures compared to infants born to the HIV - 1 uninfected women of similar socio - economic status.

Control of virus - specific CD8 + T - cell exhaustion and immune - mediated pathology by E3 ubiquitin ligase Cbl - b during chronic viral infection.

Cowpox virus inhibits human dendritic cell immune function by nonlethal, nonproductive infection.

In these experiments, the virus managed to infect and destroy only a small proportion of tumor cells directly, the researchers found, but within five days of the initial infection, the rest of the tumor began to be killed by a powerful immune reaction.

Familial hemophagocytic lymphohistiocytosis type 2 (FHL2) is a cytokine storm syndrome characterized by immune hyperactivation with viral infection due to a CD8 T cell cytotoxic killing defect secondary to a perforin deficiency.

This means our immune systems are primed to prevent another infection from the same virus, without attacking the body's own cells by accident.