Houston Methodist researchers have cracked a code in T-cells that could make autoimmune diseases and organ transplant rejection a thing of the past.
Wenhao Chen, Ph.D., a scientist in the Immunobiology and Transplant Science Center at the Houston Methodist Research Institute, and his colleagues have identified a critical switch that controls T-cell function and dysfunction and have discovered a pathway to target it.
Their findings are described in an article titled “Ablation of Transcription Factor IRF4 Promotes Transplant Acceptance by Driving Allogenic CD4+ T Cell Dysfunction” in the Dec. 19 issue of Immunity, a top medical journal of immunology published by Cell Press.
T-cells, which are a type of white blood cells that protect the body from infection, play a central role not only in infections, but also autoimmune diseases and transplant rejection. Understanding how T-cells work is of critical importance for treating these diseases. Chen and his team are doing this by systematically deleting different molecules in T-cells to check which ones are required for the T-cells to function.
What they have found is that one of the most critical molecules controlling gene expression in T-cells is the transcription factor IRF4, which is usually only found in the immune system and not expressed in other cells. Chen says IRF4 is what needs to be targeted to solve the problem of transplant rejection or to develop an autoimmunity cure.
“We found that IRF4 is an essential regulator of T-cell function,” said Chen, who is the corresponding author on this paper. “If we delete IRF4 in T-cells they become dysfunctional. In doing so, you can solve the issue of autoimmunity and have a potential solution for organ transplant rejection. You need them functional, however, to control infection. If we can find an IRF4 inhibitor, then those issues would be solved. That’s big.”
Continue reading at https://www.eurekalert.org/pub_releases/2017-12/hm-rfk122017.phpShare