Maybe
a T cell vaccine could do that.»
Around the same time, Irvine's lab developed a new type of
T cell vaccine that hitches a ride to the lymph nodes by latching on to the protein albumin, found in the bloodstream.
Not exact matches
«The holy grail is to target a piece of the virus by antibody or
t cell,» Tom Evans, the CEO of a company called Vaccitech that is working on a universal
vaccine they hope can be used to treat all strains of influenza A, told National Geographic.
His work indicates that this
cell surface marker could serve as a target for a novel brain cancer
vaccine or
T -
cell therapies engineered to recognize and kill tumors carrying that neoantigen.
And unlike current flu
vaccines, the new version also fuels a strong reaction from disease - fighting white blood
cells called
T cells.
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.
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.
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.
But he added, «We need to improve the memory responses of
T and B
cells to make longer - lasting
vaccines.»
Ultimately, researchers believe that a
T cell — boosting
vaccine by itself will not be enough to stave off AIDS.
The so - called STEP trial, sponsored by pharmaceutical giant Merck & Co. and the federally funded HIV
Vaccine Trials Network (HVTN), was the first to test the idea of stimulating the immune system's killer
T cells to hunt for the virus more aggressively, in this case using a weakened form of the cold virus to carry three genes from HIV.
Did the
vaccine not stimulate enough
T cells or for long enough?
Researchers for the past decade have focused on the
T cell approach, based on studies showing that monkeys receiving such
vaccines against simian immunodeficiency virus, related to HIV, lived longer or had lower viral levels than usual.
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.
The
vaccine harnesses the natural process of
T -
cell immunity to tumors, but enhances it to help overcome tumors» formidable defenses.
CTL119 manufacturing begins with a patient's own
T cells, some of which are removed and then reprogrammed in Penn's Clinical
Cell and
Vaccine Production Facility with a gene transfer technique designed to teach the
T cells to target and kill tumor
cells.
«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.
This seminal finding led to his recognition as an important scientist in
vaccine design, and to his inclusion as a
T cell expert in the CHAVI - ID
vaccine consortium.
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.
Then you activate the killer
T cells with the dendritic -
cell vaccine, so now you've got all your smart bombs and your cruise missiles coming in from outside.
The powerful, durable protection conferred by the candidate
vaccine is due in large part to its strong stimulation of CD4 helper
T cells, which are important for maintaining long - term antibody immunity.
In Britain, in 1991, researchers led by Jim Stott at the National Institute of Biological Standards and Control in north London, stunned their colleagues by announcing that they had apparently protected monkeys from infection with the monkey virus SIV — the simian equivalent of HIV — with a
vaccine based simply on human
T cells.
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 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.
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.
Researchers used IL - 15 to develop a whole tumor
cell vaccine to target breast (
TS / A) and prostate (TRAMP - C2) cancer
cells in animal models; results showed that tumor
cells stopped growing after the
vaccine was introduced and that beneficial effects were enhanced further when IL - 15Rα was co-produced by the
vaccine cells.
«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.»
cruzi
T cell immunity, and booster immunization would be an effective strategy to maintain or enhance the
vaccine - induced protective immunity against
T. cruzi infection and Chagas disease.»
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.
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.
T cells and B
cells reside there, and that's where you need to get the
vaccine to get an immune response.
«When you look in the blood, one in three
T cells in the blood was a
vaccine - specific
T cell, which is something you usually only see with
vaccines delivered by viruses.»
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.
In his look at the wider benefits of
vaccines, Michael Brooks describes type 1 and type 2 helper
T -
cells as...
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.
The
vaccine, which is about to go on trial in the US, aims to re-educate
T cells so that they no longer react to the dander.
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.
In his look at the wider benefits of
vaccines, Michael Brooks describes type 1 and type 2 helper
T -
cells as competitive, with levels of one going down as the other goes up (17 August, p 38).
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.
He then describes a hypothesis that
vaccines reduce allergies by boosting type 1 helper
T -
cells, reducing the number of type 2, which are geared to fight parasitic worms in the gut and are associated with allergies.
«We found that the NFkB - Pim1 - Eomes axis, an important molecular mechanism that operates in memory
T cells, could be enhanced with molecular or genetic strategies to help current
vaccines or tumor therapies be more effective.
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.
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.
That
vaccine, which included bits of beta - amyloid to arouse immune - system
T cells, cleared the clumps, but it also provoked dangerous brain inflammation in several patients.
«
Vaccine - inducedCD4
T cells lead to adverse effect in a mouse model of infection.»
«Better understanding of these mechanisms is important because increasing the quantity and quality of memory CD8 +
T cells is a key goal in developing more effective
vaccines and immunotherapeutic strategies,» said Tan.