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Making transplant rejection a thing of the past
January 7, 2018, 4:10 pm
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Autoimmune diseases and organ transplant rejection could soon be a thing of the past, suggest researchers who recently identified a critical switch that controls the processes by which certain white blood cells protect the body.

Scientists at the Houston Methodist Research Institute in the US have found that understanding T-cells — a type of white blood cells that not only protect the body from infection but also play a central role in autoimmune diseases and transplant rejection — work is of critical importance for treating these diseases.

By deleting different molecules in T-cells to check which ones are required for the T-cells to function, the researchers found that one of most critical molecules controlling gene expression is IRF4, which is usually only found in the immune system and not expressed in other cells.

When we deleted IRF4 molecule, the T-cells became dysfunctional and this could offer a potential solution to the issue of autoimmune diseases and for organ transplant rejection, said the research team.

It is the T-cells activated by exposure to antigens that become armed with IRF4 and are responsible for organ transplant rejection and autoimmunity. Specifically targeting these activated T-cells, while leaving the so-called naïve T-cells that have not been impacted by antigens, was necessary to ensure the immune system did not become compromised in its ability to fight infections.

Initial results from the study have been promising. By inhibiting IRF4 expression for 30 days —the usual timeframe required for transplant patients to remain infection free — the T-cells became irreversibly dysfunctional. In practice, this could mean prolonging a patient's ability to tolerate a transplanted organ.

"If we can find a way to therapeutically inhibit IRF4 as desired in activated T-cells, then we think most autoimmune diseases and transplant rejection will be solved," said the research team optimistically.

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