T cells protect our bodies against attackers like bacteria, cancer, and the AIDS virus. Scientists at Stanford have found a way to not only target them to threats more effectively (past work), but to allow them to act independent of other immune cells (new work).  (Source: Laplacian Files)
Why use drugs, when you can improve the body's own designs?

Evolution has bestowed mammals with amazingly complex and robust immune systems capable of fighting off a variety of foreign invaders including fungi, bacteria, and viruses.  The immune system is also capable of detecting cancerous cells -- cells in which mutations have led to uncontrolled growth which threatens to engulf normal healthy tissues.

The problem is that even nature sometimes falls short.  The immune system's T Cells, special cells used to fight extreme abnormalities such as AIDS and cancer (note, a special type of T cell fights HIV-infected T cells in AIDS), often times lack the supporting cells or can't stop the abnormality's growth fast enough.

A solution is adoptive immunotherapy, an approach in which certain T cells are harvested from the body and then cultured and exposed to the abnormality.  Kept in a tightly controlled environment they reprogram to fight the abnormality faster than in the complex human body.  The final step is to insert the cells back into the human body, now ready to fight the threat.

Unfortunately, the lack of supporting cells has hindered the promising approach.  So Stanford University bioengineering researchers developed T cells that produce their own cytokines, the special chemical that the T cells typically obtain from other immune cells.  In essence this transforms immune cells into an "army of one", which can fight the threat even if other immune cells have been killed, compromised, or are otherwise unavailable.

To prevent these cells from growing and proliferating out of control (the whole reason for the cytokine system), the researchers encoded a cellular RNA switch that confers a new sensitivity to a specific drug (different riboswitches were used, including ones sensitive to the drugs tetracycline and theophylline).  The T cells only produce their own cytokines when exposed to this drug.

The super-cells featured 24 percent more live cells, when cultured, than normal T cells.  They also had a 50 percent reduced death rate.

Christina Smolke, PhD, assistant professor of bioengineering proclaims, "This is an integration of a cell-based therapy application with new synthetic biology tools that have come up from foundational research.  The unique aspect is that we're taking new tools for controlling cell function and gene expression, and looking at them in the context of a specific and clinically relevant system."

After solving the problem of enabling the T cells to act all alone as splinter cell agents, only one additional problem remains -- finding the ideal drug-switch combo to keep them on when needed, and to shut them off once the attack on the disease is complete.

If that puzzle can be solved, the therapy may prove a non-toxic approach to fight a variety of diseases such as cancer and AIDS that are countered in healthy immune systems by T cells.

The new work was published in the journal 
Proceedings of the National Academy of Sciences.  It was funded by the City of Hope's Comprehensive Cancer Center, the National Science Foundation and the Alfred P. Sloan Foundation.

"There is a single light of science, and to brighten it anywhere is to brighten it everywhere." -- Isaac Asimov

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