Sentences with phrase «where t cells»

As the name implies, cellular immunity works on a cellular level where T cells are able to detect which of our cells contain the unwanted virus and work to destroy it.

The thymus is where T Cells mature and as such it plays an important role in immunity.

Also the site where T cells are «educated» to destroy harmful invaders in your body.

«While transient disruption of this pathway may have therapeutic benefit because it temporarily «revs up» the immune response, permanent loss of PD - 1 signals seems to result in a «flame out» where T cells can't sustain higher level activation and become more dysfunctional,» Wherry says.

Epitopes are displayed on the surface of circulating immune cells and are where T cells bind antigens to fuel the immune response.

«This could be especially useful for the treatment of solid tumors where T cell therapies have been largely ineffective,» Roybal said.

Not exact matches

-LCB--LCB- «Wi - Fi can provide you with added coverage in places where cell networks don \» t always work - like basements and apartments.

♦ One of the selling points of Wyoming Catholic College, announced on a T - shirt I saw a student wearing: «The only school in America where you can't have a cell phone but you can have a gun.»

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.

The long - term persistence of CD8αα + T cells where initial infection occurs may explain why patients have asymptomatic recurrences of genital herpes because these cells constantly recognize and eliminate the virus, according to Jia Zhu, Ph.D., corresponding author, research assistant professor in Laboratory Medicine at the University of Washington and an affiliate investigator in the Fred Hutch Vaccine and Infectious Disease Division.

Now, the team has examined whether sepsis has the same impact on tissue resident memory T cells (TRM), which do not circulate but stick to the skin, lungs, and gut — where infections often enter the body.

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.

Scientists examined the DEJ for T cell activity because this is where the genital herpes virus multiplies after reactivating and traveling from its hiding place in the body's sensory neurons.

New HIV particles are released into the bloodstream, where they target other T - cells, and the process starts all over again.

But the bottom line is that about two thirds of all T cells reside in the lymphoid tissue of the gut, where the virus spreads after exposure, even before it shows up in blood.

Dr. Sade started her scientific career as a research fellow at the National Centre for Biological Sciences in Bangalore, India, where she investigated regulation of the survival and death of T cells.

They internalize them and migrate to the nearest lymph node, where they present them to other immune cells, namely T - cells.

Killer T cells (green) surround a cancer cell (blue), where they will deliver the death blow via chemicals stored in vesicles (red).

Many cancers take control of regulatory T cells to suppress the immune system, creating an environment where tumors can grow without being detected.

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.

Built to annihilate any cell carrying weak EBV, the T cells are injected back into the patient's body, where they efficiently kill the cancer with nary a side effect.

In a decades - long game of hide and seek, scientists from Sydney's Westmead Institute for Medical Research have confirmed for the very first time the specific immune memory T - cells where infectious HIV «hides» in the human body to evade detection by the immune system.

Researchers are also working to develop a trial where they will reprogram CAR T cells to identify the CD19 and CD22 proteins simultaneously, enabling them to target the cancer cells from more than one angle with the initial round of T - cell immunotherapy.

In the right SEM image, T cells (in blue) bind to a section of a completed antigen - presenting cell - mimetic scaffold (in brown), where they are instructed to multiply and are kept alive for future use in T cell therapies.

While the research showed that the T cells left the bloodstream, where they went is a mystery.

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

«The next stage would be to repeat the study in primates, a more suitable animal model where HIV infection induces disease, in order to further demonstrate elimination of HIV - 1 DNA in latently infected T cells and other sanctuary sites for HIV - 1, including brain cells,» Dr. Khalili said.

«These animals carry latent HIV in the genomes of human T cells, where the virus can escape detection,» Dr. Hu explained.

Once the engineered T cells have multiplied, they're infused into the patient, where they go to war.

As the infection progresses, adaptive immune cells called T cells move to the area of infection, where they detect and kill infected cells.

«We now know that T cells parked where they reside in the skin are the ones eliciting the most potent anti-tumor response,» explains Paulos.

The next step is a bigger trial where the researchers will combine romidepsin activation of hidden HIV with a vaccine (vacc - 4x) to strengthen the ability of killer T - cells to fight hiv virus.

With a better «nose» for these chemicals, the altered T cells make a beeline for the outer layer of the skin, where they began destroying defective and infected cells, the team reports in the February issue of Nature Immunology.

T cells and B cells reside there, and that's where you need to get the vaccine to get an immune response.

«We could potentially transfer these specialised super potent killer T cells into patients, or we could treat patients with proteins that can drag these specialised killer T - cells into the right spots, specifically to the hot spots where HIV can hide on antiviral treatment,» Professor Lewin said.

Antibody responses are initiated in lymph nodes close to the site of initial infection (so - called draining lymph nodes, or DLNs), where antigen - presenting cells, helper T cells, and antibody - producing B cells migrate to and interact to form so - called «germinal centers» and produce a highly specific antibody response.

In cases where there are lots of T cells in the vicinity of a tumor, or where tumor cells have undergone large numbers of mutations, which creates additional targets for immune sentries, T cells will signal a full - fledged immune response to the cancer.

Memory T cells regularly patrol the lungs, where they distinguish harmless challenges like cat dander or tree pollen from more serious insults like respiratory viruses or pathogenic bacteria.

The modified T cells are then infused into the patient's bloodstream, where they target and kill cancer cells.

Celiac disease is an autoimmune disease where special immune system cells, called gluten - specific T cells, have an extraordinarily strong inflammatory reaction to gluten.

«Some of the best examples of this are what are called checkpoint inhibitors, where essentially cancers put up stop signs [that prevent] T - cells from killing them.

In 2008, he joined the group of Caetano Reis e Sousa at the Cancer Research UK (CRUK) London Research Institute and later joined the Francis Crick Institute, where he was awarded Marie Curie and EMBO long - term postdoctoral fellowships to investigate innate immune receptors and signaling pathways that trigger dendritic cell activation and drive T - cell responses against viruses or tumors.

He received his Ph.D. in immunology at the Gulbenkian Institute of Science in Portugal, where he studied regulatory T cells, working with Jocelyne Demengeot and António Coutinho.

To develop new, targeted treatments to eliminate these residual infected cells, we need to find exactly where in the CD4 T lymphocyte population the virus hides.

When there is too much calnexin, this wall gives angry T cells access to the brain, where they destroy myelin.»

These cells travel to the spleen, where they present alarmins (or other antigens) to T cells.

The mechanism used by Notch to regulate Myc in B cells is distinct from the mechanism used in other cell types, such as T cells, where Notch also regulates Myc.

By developing blood biomarkers and «immunologic signatures» related to antigen - specific T - cell responses, the researchers hope to identify individuals with latent TB infection who are at greatest risk for progression to active disease, allowing development of prevention strategies to target those at highest risk in areas with high rates of infection (usually low - and middle - income countries), as well as high income countries such as the U.S., where factors such as recent infection and HIV co-infection are associated with an increased risk of progression to active TB.

«Until now, it often has been a real mystery which antigens T cells are recognizing; there are whole classes of disease where we don't have this information,» said Michael Birnbaum, a graduate student who led the research at the School of Medicine in the laboratory of K. Christopher Garcia, the study's senior author and a professor of molecular and cellular physiology and of structural biology.

Although there is new data coming from Dr. Michel Sadelain's lab and others where they have made a molecule that may work as a CAR T cell that would then bind to NY - ESO - 1 peptides displayed on the surface of a tumor cell.