«IL - 28B is a key regulator of B - and T -
Cell vaccine responses against influenza» by Adrian Egli et al. published in PLOS Pathogens on Thursday 11 December 2014.
Not exact matches
To fend off HIV, researchers introduced one
vaccine (ALVAC) to induce a T
cell response — thereby alerting the immune system — and another (AIDSVAX) later to spur an antibody
response.
«Similarly, triggering extra production of particular dendritic
cells could improve the immune
response to infections or
vaccines.
But he added, «We need to improve the memory
responses of T and B
cells to make longer - lasting
vaccines.»
Davis will use his findings to figure out a way to match specific immune
cells to
vaccine response.
Essentially, he's looking for immune
cells with barcodes that proliferate in individuals with a good
response, as opposed to those in whom the
vaccine is ineffective.
It is the stuff of dreams for flu scientists, but it could be within reach if a new type of
vaccine that elicits an immune
response from white blood
cells is combined with traditional
vaccines.
The personalized
vaccine is made from patients» own immune
cells, which are exposed in the laboratory to the contents of the patients» tumor
cells, and then injected into the patients to initiate a wider immune
response.
The
vaccine also induced a sharp rise in CD4 T -
cells, whose job is to mobilize the antibody
response and other immune elements against viral infections.
Crotty says the ability to measure Tfh
cells in the blood will assist AIDS
vaccine researchers by serving as an indicator of antibody
response.
«We've shown that a specific type of these
cells, known as follicular helper T (Tfh)
cells are not only necessary, but are a limiting factor that differentiates between an average and a potent antibody
response to HIV,» says Crotty, a scientific collaborator with the Center for HIV / AIDS
Vaccine Immunology & Immunogen Discovery (CHAVI - ID), a major research consortium led by The Scripps Research Institute.
La Jolla Institute scientist Shane Crotty, Ph.D., a respected
vaccine researcher and member of one of the nation's top AIDS
vaccine consortiums, showed that certain helper T
cells are important for triggering a strong antibody
response against HIV, the virus that causes AIDS.
In particular, the researchers must ensure that their
vaccine does not result in an autoimmune
response to
cells that produce ghrelin, which could trigger severe swelling and inflammation.
To fend off HIV, researchers introduced one
vaccine (ALVAC - HIV) to induce a T
cell response — thereby alerting the immune system — and another (AIDSVAX B / E) later to spur an antibody
response.
And the key to
vaccine success is that, afterward, the immune system starts to create fast -
response infection fighters called memory
cells that will circulate throughout the body and be able to recognize (and fend off) that same pathogen in the future.
Significantly, the
vaccines were able to stimulate both arms of the immune system — a T
cell response and an antibody
response.
In theory, the ideal
vaccine might mimic both antibody and T
cell responses to block an infectious disease.
But in truth, most (26 of 28
vaccines currently licensed for human use) stimulate primarily a B -
cell or antibody
response, which in many cases is sufficient.
«Additionally, this provides evidence needed to begin investigating a
vaccine in human cancer clinical trials to determine whether genetically modified tumor
cells producing IL - 15 and IL - 15Rα may induce anti-cancer
responses.»
«Our new work suggests that
vaccines targeting either virus could be engineered to induce both T
cell and antibody
responses effective to protect people in these areas.»
Cincinnati Cancer Center (CCC) and UC Cancer Institute researchers have found that a
vaccine, targeting tumors that produce a certain protein and receptor responsible for communication between
cells and the body's immune system, could initiate the immune
response to fight cancer.
The
vaccine generated a pool of TH1 CD4 + T
cells (also called helper T
cells) that are necessary for an effective antibody
response as well as a stable pool of CD8 + T memory
cells.
T
cells and B
cells reside there, and that's where you need to get the
vaccine to get an immune
response.
Analyses of RV144 volunteers revealed that particular
vaccine - induced immune
responses, including production of certain antiviral antibodies and CD4 + T
cell responses to HIV's outer shell, or envelope, correlate with reduced HIV infection.
«The idea basically is that a
vaccine should induce antibodies T
cells immune
response, that would neutralise HIV in all of its forms,» explains Ulrich Fruth,
vaccine development and evaluation team leader at the World Health Organisation, in Geneva, Switzerland.
«
Vaccine used to treat cervical precancers triggers immune
cell response.»
The influenza specific T - follicular helper
cell response varied based on trimester of pregnancy in which the
vaccine was given.
What's more, IL - 33 and the DNA
vaccine augmented immunological
responses in both CD4 helper T
cells and CD8 killer T
cells, with a large proportion of CD8 killer T
cells demonstrating a further improvement in the ability of DNA
vaccines to drive the immune system to kill tumor
cells in animals.
Vaccine immunology is poorly understood in pregnancy and Tfh
cell expansion has been shown to be a predictor of
response to influenza vaccination outside of pregnancy.
«The development of DNA - based
vaccines with cytokine adjuvants has emerged as particularly promising for inducing antiviral and anti-tumor,
cell - mediated immune
responses.»
The investigators also said the
vaccine did not have the unwanted consequence of altering the number of T - regulatory
cells, which suppress immune system
responses.
The team showed that IL - 33 can further enhance the
response of memory T
cells, the long - lived
cells that can patrol and protect the body from infections and cancers, when given with a DNA
vaccine compared to a
vaccine without IL - 33.
But Nabel noticed that this modified adenovirus alone stimulated rapid antibody production, and even produced a T -
cell response, although at a lower level than the DNA
vaccine.
The new technique, pioneered by Wilson and fellow researchers at the Emory University School of Medicine in Atlanta, saves time by using antibodies produced by so - called B
cells (white blood
cells that produce and then ferry them to infection sites to battle invading germs) in
response to
vaccines instead of to actual infections.
Instead of stirring up powerful T
cells through an injected amyloid
vaccine, they used a nasal spray containing two drugs that provoke a less robust but more manageable immune
response.
When injected into mice that were then given a subsequent injection of lymphoma
cells, the 3D
vaccine generated a potent immune
response and delayed tumor growth.
While this approach has had some clinical success, in most cases, the immune
response resulting from dendritic
cell vaccines is short - lived and not robust enough to keep tumors at bay over the long run.
And when they pre-treated immune
cells from vaccinated major allele carriers with a molecule that inhibits the receptor that is normally stimulated by IL - 28B, they saw a stronger antibody
response after the
cells were stimulated with influenza
vaccine.
The
vaccine sets off an immune
response using a piece of a protein, called PR1 peptide, found on the surface of leukemia
cells.
For this, a
vaccine response more rapid than the spread of the virus and one that can stop damage to the
cells is sufficient.
«While the prevailing wisdom would suggest that
vaccines that make really strong CD4 T
cell responses would, in their helper capacity, strengthen the
responses of both antibodies and CD8 T
cells, we often see that
vaccines and viral infections seem to generate fewer CD4
responses than they do CD8
responses,» says Penaloza - MacMaster.
Up until now, efforts in generating a
vaccine against TB have been mainly focused on T
cells (
cells from the adaptive arm of our immune
response with memory capacity), with very disappointing outcomes in both pre-clinical as well as clinical trials.
The
vaccine is unique to the individual participant and is engineered to trigger an immune system
response to kill tumor
cells that may remain following surgery.
Significant advances also have been made in understanding T -
cell responses that may be important to
vaccine - induced immunity against HIV.
It included a 1994 report from the Institute of Medicine that said it was biologically plausible for a
vaccine to «induce... an autoimmune
response... by nonspecific activation of the T
cells directed against myelin proteins.»
The researchers found that the personal
vaccine induced a focused T
cell response against several tumor neoantigens, beyond what is normally seen in
response to existing immunotherapies.
Cancer
vaccines, engineered to continue to train T
cells to mount a strong immune
response against your cancer, also haven't been very effective at mounting a strong fight, says He, and likely one weak point is the lack of strong receptors.
Most importantly, many of the T
cells were able to recognize the tumor
cells directly, demonstrating that the
vaccine had triggered a tumor - specific immune
response that could target the patient's tumor.
The
vaccine was aimed at generating
responses to the neoantigens from T
cells of two kinds — CD8 + killer
cells and CD4 + helper
cells.
A personal cancer treatment
vaccine that targets distinctive «neoantigens» on tumor
cells has been shown to stimulate a potent, safe, and highly specific immune anti-tumor
response in melanoma patients, report scientists from Dana - Farber Cancer Institute and the Broad Institute of MIT and Harvard.