In fact, one of the mysteries remaining for BanLec work is just
how the T cells of the immune system actually attach to it.
A study led by researchers at Stanford's School of Medicine reveals
how T cells, the immune system's foot soldiers, respond to an enormous number of potential health threats.
By studying
how the T cells responded, the group learned that the cells were primed to fight a different strain than the one attacking them.
«We have revealed novel components and connections in the regulatory network underlying
how these T cells mount an immune response,» said study co-leader Kai Tan, PhD, of the Center for Childhood Cancer Research and the Departments of Pediatrics and Biomedical and Health Informatics at CHOP.
One of immunology's great unknowns was
how T cells recognized the antigen that marked an invader for destruction.
The algorithm was built using tools the researchers developed to define
how T cell receptors recognize a part of the antigen called the epitope.
Howard Hughes Medical Institute researchers have discovered
how the T cell, the body's chief immune - system warrior, organizes signaling molecules that mobilize the weaponry used to attack foreign...
Not exact matches
Hoping to learn something about
how the human body defends itself against cancer, he had zeroed in on a complex regiment of lymphocytes called
T cells, common to the immune systems in both mouse and man.
How CAR -
T Works CAR -
T therapy extracts your own
T -
Cells.
«Ultimately, we needed 20 years to learn
how to supercharge these
cells to deliver anticancer activity,» says Arie Belldegrun, president and CEO of Kite Pharma in Santa Monica, California, which is assessing CAR
T cells in six trials for B
cell leukemia and lymphomas, and glioblastoma.
For instance, specific anti-
T-cell therapies don'
t work at all for rheumatoid arthritis (RA), and Edwards doesn'
t think
T -
cells explained
how the disease persisted.
«Our lab specializes in developing novel genetic methodologies to study
T cell repertoires, but we had never applied this technology to study
how the immune system responds to an infection,» says Emanual Maverakis, M.D., associate professor of dermatology at the University of California, Davis School of Medicine.
Their paper, which appears in Nature Communications, describes
how an immune
cell recruited to the tumor induces the programmed suicide, or apoptosis, of the killer
T cells harnessed by many immunotherapies.
«With this algorithm we have a system to identify critical features of
T cell receptors that recognize the same antigen and
how they interact.
This is
how treatments based on a type of white blood
cell called
T -
cells are curing some cancers, rather than just slowing their advance (see «Cancer meets its nemesis in reprogrammed blood
cells «-RRB-.
This microscopic image of fixed
cells shows
how a dendritic
cell presents the messenger substance interleukin 6 (IL - 6) to a
T cell.
Nadeau stumbled upon one study, in mice, describing
how environmental factors can tag Foxp3 with chemical markers that tell
T -
cell precursors to switch the gene on or off.
Although Coley couldn'
t explain precisely why or
how his toxins worked, modern immunotherapy treatments help
T -
cells in the immune system to recognize specific cancer
cells and attack them.
In the meantime, the MUSC team, led by Yu, will continue their work and try to extend the current findings by investigating
how other miRs may be involved in regulating
T - and B -
cell function during allogeneic BMT.
«The mechanism for
how miR -17-92 regulates
T - and B -
cells was very consistent.
«We already know
how to stimulate the immune system to make CD8
T cells by vaccination.
Associate Professor Palmer said that this next - generation test showed that HIV hides in the body's immune memory
T -
cells, which is
how it avoids detection from the immune system.
Effector memory
T -
cells are the
cells in the body that «remember» previous infections and
how to defeat them.
While a range of cellular markers of exhaustion, such as PD - 1 and TIM3, have been characterized and are even the target of cancer immunotherapy drugs, the molecular details of
how CD8
T cells switch gears were unclear.
This result reflected earlier findings that ILC and
T cell subclasses produce similar sets of cytokines, but also revealed differences in
how the two
cell types control the activities of these key immune response genes.
To determine what sets ILCs apart from
T cells, Dr. O'Shea's team looked to the foundation of a
cell's identity — its genetic information, which provides detailed instructions for
how a
cell functions.
«Recent successes in cancer immunotherapy — in the form of immune checkpoint inhibitors and adoptive
T cell transfer — demonstrate
how activated immune
cells can eradicate tumors, but until now we didn'
t fully appreciate immunosurveillance or the role of adaptive immunity in tumor formation,» said senior author Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology at UC San Diego School of Medicine.
«ILCs were discovered less than a decade ago, but the parallels between them and
T cells will enable us to more quickly understand
how they work and to develop ways to enhance or inhibit their function in treating a variety of immune and inflammatory diseases.»
The results confirmed the team's previous finding that the replicative capacity of the newly established virus drives
how quickly infected individuals» levels of CD4
T cells declined.
The researchers are now looking at
how ICOS signals can be altered to diminish autoimmune disorders and augmented for more effective vaccine development, and are beginning research on
how ICOS signaling may benefit Chimeric Antigen Receptor -
T cell (CAR -
T) therapies, which involves engineering of patient's own immune
cells to recognize and attack their cancers.
Geneticist at the University of Toronto in Canada, the first to clone the
T -
cell receptor, discusses
how a scientific breakthrough can change your life:
«The results show for the first time
how NFkB signaling regulates the production of memory
T cells during infection.
«We studied
how the Sox2 gene is turned on in mice, and found the region of the genome that is needed to turn the gene on in embryonic stem
cells,» said Professor Jennifer Mitchell of U of
T's Department of
Cell and Systems Biology, lead invesigator of a study published in the December 15 issue of Genes & Development.
Researchers are studying
how NK
cells recognize cancer
cells as abnormal and
how other
cells, known as regulatory
T cells, can command NK
cells to hold their fire, in order to prevent them from attacking the body's own tissues.
When the research team activated the human
T and B
cells, simulating
how these
cells would respond when presented with a pathogen, the Xist clouds reappeared.
Kipnis and his colleagues wondered
how smart mice would be if they had a normal supply of
T cells everywhere in their bodies except the meninges, so he injected a compound into mice that prevented
T cells from reaching the meninges.
Some researchers think the new findings could shift the field's view on
how the body handles self - reactive
T cells.
This study showed
how HIV attempts, but fails, to productively infect most of the immune system's CD4
T cells.
To understand
how the different alleles influence the immune response to vaccination, the researchers next looked in more detail at immune
cells from 47 of the patients (34 had two major
T alleles, and 13 had at least one minor G allele).
In an effort to further define the importance of GATA - 3, researchers at the University of North Carolina have traced
how the protein performs important functions in CD8 +
T -
cell type of the immune system.
After all, that would seem to offer a neat explanation for
how HIV causes the collapse of the immune system by suppressing
T cells.
We believe that each dog breed may correspond to one type of B - or
T -
cell lymphoma and so studies within and between breeds gives us a unique possibility to understand
how the genetic background affects what type of tumor develops, and
how its progression is regulated,» says Ingegerd Elvers.
«Our studies have investigated and identified the root cause of AIDS —
how CD4
T cells die,» said Gladstone Staff Research Investigator Gilad Doitsh, PhD, who is the Nature paper's lead author, along with Nicole Galloway and Xin Geng, PhD.
The study didn'
t test humans, and it doesn'
t solve all of motherhood's mysteries, Way acknowledges, but he hopes his team's future studies will determine
how long the regulatory
T cells» memory lasts and
how to extend or boost the response.
A recent paper in the experimental biology publication The FASEB Journal describes
how peptides found in hookworms inhibit the proliferation of effector memory
T cells, which, unlike regulatory
T cells, can actually trigger inflammation.
«Our lab is interested in understanding
how T -
cell identity is established,» Vahedi said.
«The retraction states that Mignot and his colleagues were unable to replicate the results of the ELISpot assay, a widely used method for measuring
how immune system
cells such as
T cells respond to fragments of foreign proteins, called antigens,» Underwood writes.
«Typical food triggers creation of regulatory
T cells: Researchers document
how normal diet establishes immune tolerance conditions in the small intestine.»
«The collapse of the CD4 +
T -
cell system is the cardinal feature of AIDS,» Goldsmith observes, «so understanding which subsets of
T cells can be infected is important in providing a clear picture of
how HIV reduces the number of
T cells.»
Scientists are not exactly sure
how HIV causes the CD4 +
T cell population to activate and crash.