A long noncoding RNA whose function was previously unknown turns out to play a vital role in mobilizing the immune response following a bone marrow transplant or solid organ transplantation. This RNA molecule, cataloged in scientific databases simply as Linc00402, helps activate immune defenders known as T cells in response to the presence of foreign human cells, according to a new study by researchers at the University of Michigan Rogel Cancer Center and Michigan Medicine.

The investigation, which included samples from more than 50 patients who underwent a bone marrow or heart transplant, suggests inhibiting the RNA therapeutically might improve outcomes for transplant recipients. Their findings appear in Science Translational Medicine.

"We see a lot of graft-versus-host disease—or GVHD—which is a potentially fatal complication that can happen after transplant when T cells in the donor's blood see the transplant recipient's cells as invaders and attack them," he says. "Unfortunately, the medicines we use to prevent GVHD suppress the immune system and can raise the risk of a cancer relapse or infection, and they also have other side effects."

In taking a deep dive into the biology, Peltier and his colleagues hoped to find a way of targeting just the problematic components of the immune system that cause GVHD. So, unlike a lot of RNAs, which are expressed in all kinds of cells by all kinds of living things, long noncoding RNAs offer the possibility that we might be able to target them in a relatively unique and disease-specific way, he says.

Meaning: If doctors can find a way to zero-in and short circuit just the T cells' tendency to get aggressive in response to the transplant, they may not need to suppress the patient's immune system in a more general way that leaves them susceptible to infection or a regrowth of their cancer.

Regards

John
Editorial Assistant
Immunogenetics Open Access