What happens
when T cells detect suspicious activity in the body?
When T cells were donated by young mice, the anti-NP response in GC was dominated by the canonical V186.2 gene, even if the responder B cells came from aged donors.
And
when T cells do destroy tumor cells, those cancerous cells release potassium — which in turn destroys T cells and keeps them from going after additional tumor cells.
The findings have implications for the design of cancer vaccines and what are called adoptive T cell therapies;
when T cells are collected from a patient and grown in the laboratory, increasing in number before they are given back to the patient to help the immune system fight disease.
When T cells expressing LIGHT were introduced into the mice, lipid levels rose, both when the mice were fed a regular diet, and also when fed a high - fat, high - cholesterol diet.
When the T cells kill the tumor cells, they trigger inflammation, and that causes the fever.
«The antibody - driven innate response creates an environment such that
when the T cells come in, they can kill the tumor.
When the T cells stay resting, it's referred to as being immune quiescent.
When T cells respond to a pathogen, they proliferate, and a fraction of their progeny goes on to form long - lived memory cells.
When the T cells of your immune system are forced to deal over time with cancer or a chronic infection such as HIV or hepatitis C, they can develop «T cell exhaustion,» becoming less effective and losing their ability to attack and destroy the invaders of the body.
The problem is that
when T cells are allowed to attack, they can destroy both cancer cells and healthy cells, leading to a wide array of side effects.
When T cells specifically recognize influenza virus proteins, they then begin to proliferate in the lymph nodes around the lungs and throat.
This discovery led the researchers to identify a mechanism where ileal Crohn's disease appears to be induced by bile acids
when T cell adaptation does not occur the way it should.
When a T cell detects one, it morphs into a fighting machine, zapping invaders with lethal chemicals, multiplying into an army of identical killers or signaling other immune - system troops to join the attack.
Not exact matches
The athletic adults also appeared to have healthier and younger - looking immune systems, at least
when it came to an organ called the thymus that's responsible for generating key immune
cells called
T cells.
In December, SQZ partnered with global pharma firm and cancer treatment leader F. Hoffmann - La Roche in a deal that could be worth $ 500 million or more — a large undisclosed upfront payment, and additional sums
when SQZ meets certain milestones — to speed up the development of its technology specifically to inject a person's immune
cells with a protein to activate a «killer
T»
cell response to fight off cancer.
This lectin binds to the membranes of
T -
cells in the body and interferes with cellular metabolism
when consumed in sufficiently large quantities (SOURCE).
Some of the viruses that can be within breast milk are: HIV — Human Immunodeficiency Virus (AIDS) HTLV - 1 Human
T -
Cell Leukemia Virus Type I CMV — Cytomegalovirus
When you are using a previously owned breast pump you create the risk of cross contamination.
A pre-clinical study of two drugs designed to boost
T cell performance, has revealed the agents,
when give in combination, may enhance the immune system's ability to kill melanoma tumors deficient in the tumor suppressor gene PTEN.
When the dendritic
cells are activated, they train
T cells — their allies in the adaptive arm of the immune system — to attack cancer
cells anywhere in the body, whether at the site of the original tumor or distant metastases.
The mice produced more memory
T -
cells, which kick in
when bugs come back, than mice not given the drug.
«We were looking at the amino acid sequences of
T cell receptors
when Tomer asked what the corresponding epitope was for a particular receptor,» Thomas said.
A study published on December 3rd in PLOS Pathogens suggests that one such strategy blocking the PD - 1 / PD - L1 pathway works, but only
when the overall HIV load is low and regulatory
T cells cooperate.
However,
when pathogenic
T cells recognize autoantigens, i.e. elements of the body's own substances such as the myelin sheath, these
T cells trigger an autoimmune disease.
«
When syndecan - 4 is lacking, the APCs can not find their way to the
T -
cells and consequently can not activate them.
«The
T cells do not always become pathogenic
when IL - 6 is secreted.»
«Our observations suggest regulatory
T cells can also become functionally exhausted
when they lose LKB1 signaling.»
When they examined mice genetically incapable of producing Helios, they found the animals beset by a
T -
cell and antibody attack on normal tissue.
When dendritic
cells not only signal myelin as a «target substance,» but also secrete the messenger substance IL - 6, a sort of molecular switch is flipped in the
T cells.
An isoform of amphiphysin 2 concentrated at
T - tubules induced tubular plasma membrane invaginations
when expressed in nonmuscle
cells.
For now, the treatments are approved for use only
when other treatments have failed, but someday CAR -
T cell therapy could be the first treatment doctors try, he says.
When these pre-programmed
T cells recognize an infection, they destroy the invader.
When the
cells are reinfused, they stimulate
T cells to attack the patient's tumors.
The
T cell's self - destruct program is turned on
when a molecule on its surface, called Fas, binds to a protein called Fas ligand.
When researchers added the immune
T cells to the fibroblasts, the tumor
cells began to die off.
But
when PD - 1 binds to proteins called PD - L1 and PD - L2 on the surface of certain cancer
cells, the
T cells essentially become paralyzed: the immune attack on cancer is called off.
The researchers found that the protein, called VRC07 - αCD3, triggered the activation and killing of latently HIV - infected helper
T cells when the
cells were taken from patients on antiretroviral therapy and then incubated in the lab with the patients» own killer
T cells.
The
T cell migration halted again
when the team added a chemical that blocks the IGF - 1 receptor, the authors report 23 August in the Journal of Immunology.
In addition,
when a subcutaneous tumor began to recur two months after CAR
T -
cell therapy and a surgical biopsy was performed, the CAR
T -
cells spontaneously re-expanded and the tumor again went into remission, and phenomenon that had not previously been reported.
When they find an intruder, the dendritic
cells brandish a sample (think of a most - wanted poster) and rush to the lymphatic system, where they present it to
T cells, whose role is to form a posse and fan out through the body to hunt down and kill any proteins that look like the poster.
When spleen CD4 +
T -
cells were transferred from heart - attack donor mice to naïve recipient mice, they induced long - term left ventricle dysfunction, fibrosis and enlargement, hallmarks of heart failure.
When the toxin builds up, it destroys
T and B lymphocytes, the body's infection - fighting immune
cells.
But controversy arose in 1991,
when a team led by pharmaceutical researcher Peter Linsley identified another protein molecule, CTLA - 4, which closely resembled CD28 and was found only on activated
T cells.
Memory
T -
cells are the
cells that become primed to mount a specific immune response
when an antigen from a pathogen or injured tissue appears a second time.
HIV infects the body by corrupting
T cells that are mobilized by the immune system
when the virus enters a person's body.
Researchers found that some subsets of
T cells are reduced from the bloodstream during sleep
when risk of infection is low.
Several years ago,
when Feske and his colleagues were at another institution, they were the first to identify ORAI1, a new calcium channel, which is essential for calcium influx and
T -
cell function.
When activated, these checkpoints can turn a
T cell from a bristling warrior ready for a fight into a dozing sentinel — and cancer...
The antibody blocks CTLA - 4, a protein switch on the surface of
T cells that,
when turned on, dampens their activation.
When a young (or naive)
T cell is in a resting state, it uses oxygen to «breathe.»