Keeping immune cells engineered to kill cancer from killing everything else

A T cell, the basis for immune therapies against cancer. (credit: NIAID)

One of the more exciting developments in cancer research involves tweaking the immune system to attack cancer. It's possible to engineer the immune system's T cells to attack and kill tumor cells based on the specific proteins those tumors produce. It's a relatively new anti-cancer therapy, but initial tests have shown it to be clinically effective, especially against leukemias (wherein B cells become cancerous).

But as with chemotherapy, the side effects are severe—when immune cells run amok, bad things can happen. The T cells raised to fight the tumor can elicit what's called a "cytokine storm," setting off an intense immune reaction. They can also overstep their bounds to kill all of a patient's B cells rather than just the cancerous ones.

One of the most promising strategies employed to alleviate these side effects is to make the anti-tumor T cells dependent upon a ”switch.” Rather than using one of the T cell's normal receptors to latch on to cancer cells, it's possible to engineer one that only sticks in the presence of an exogenous small molecule—drug-dependent killing, in effect. This way, the T cell is only activated in the presence of the switch molecule, which can be administered or removed at will or dosed as desired.

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