The laborious process entails isolating a patient's T cells and inserting a new gene.
The T cells, Lieberburg says, seem to be the culprits behind the brain inflammation.
In a cruel twist, the body's disease-fighting T cells attack healthy skin cells, misidentifying them as foreign.
It will be tricky engineering T cells to survive inside the body long enough to destroy the cancer.
But it also spurred the body to send out T cells, predatory immune cells that hunt down infection.
He is one of a handful of researchers attempting to reprogram a patient's own T cells to attack cancer.
Normally, T cells travel throughout the body to detect and fight off foreign substances, such as viruses or bacteria.
When they hooked up with CD-2, the decoys prevented the real LFA-3 from binding to and activating the T cells.
In 1987 Biogen and Harvard University scientists were experimenting with a receptor called CD-2, situated on the surface of T cells.
Someday he envisions cancer centers storing giant banks of premade T cells to match the patients' bone marrow and tumor types.
One reason for the limited response rate may be that some patients' T cells do a poor job of recognizing melanoma.
Ultimately, researchers will likely want to combine it with one of the vaccines being developed to stimulate production of killer T cells.
But during an illness, or when the immune system goes haywire in autoimmune diseases such as diabetes, the attacking T cells take over.
The modified T cells are grown outside the body for several weeks until billions of them are ready and are then injected back into the patient.
The biggest is why the new technique is able to make T cells unresponsive to just the specific tissues that are initially transplanted.
In addition, other types of cancer can interfere with the activation of "killer T cells" - immune cells which arrive to destroy tumour cells.
Just what causes T cells to malfunction in people with psoriasis isn't entirely clear, although researchers think genetic and environmental factors both play a role.
If you have psoriasis, however, the T cells attack healthy skin cells by mistake, as if to heal a wound or to fight an infection.
Their experiments on mice showed the virus impaired the ability of a specific part of the immune system, called regulatory T cells, to calm inflammation.
"We thought maybe we should look at T cells, " says Alice Gottlieb, a psoriasis expert and director of clinical research at UMDNJ-Robert Wood Johnson Medical School.
To do this, they used antibodies designed to bind to and thus decommission the molecules on T cells that are used to shake hands with antigen-presenting cells.
They found that T cells went into action when CD-2 bound itself to a counterpart molecule, LFA-3, on the surface of cells that escort antigens to their death.
The antibodies seem to respond to only a quarter of the beta amyloid molecule, and the rest of the molecule seems to call the T cells into action.
Not only did it increase production of a chemical which attracts "killer T cells" to the tumour site, it also switched these cells into an active state once they arrived.
The idea is that the vaccines will train T cells to spot cancer, while the antibody will make sure the T cells remain activated long enough to do their dirty work.
Pfizer's drug tremelimumab and Bristol-Myers Squibb's ipilimumab are antibodies to a protein called CTLA-4 (cytotoxic T-lymphocyte antigen-4) that acts as an emergency brake to prevent killer T cells from attacking healthy tissue.
Antigen-presenting cells collect fragments of proteins from foreign bodies (normally pathogens, such as viruses and bacteria, but also transplanted organs) and show these to T cells, in order to tell them what to attack.
Researchers believe these new antibodies promote the production of a mysterious class of immune system cells called regulatory T cells that act as peacekeepers to ensure the rest of the immune system's soldiers remain under control.
It was hoped that time would allow the developing T cells in the thymus to be "introduced" to the donor tissue, so that when they were circulating around the body they would not attack the donor organ.
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