Generally, T cells, the policemen of the body, activate immune responses upon finding infected or diseased cells, but some T cells respond the same way to normal cells in the body. If unchecked, such T cells can cause autoimmune diseases such as psoriasis, rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis. These self-reactive T cells are a recently discovered type of T cell, the TH17 cell. Preventing young T cells from becoming TH17 cells is of major interest as a means to treat autoimmune diseases.
In a recent study published in Nature, scientists have uncovered a new aspect of TH17 cell development, suggesting a new approach to halt their evolution.
“Until now, the approach to inhibiting TH17 cell development wasn’t entirely specific—it could hamper responses to infection or increase risk of lymphoma,” said Fraydoon Rastinejad, PhD, a professor in SBP’s Integrative Metabolism Program and a contributor to the research. “With this added level of information we can design novel approaches to more specifically manage these cells and avoid unwanted interference with the immune system.
The study, led by Dan Littman, MD, PhD, of NYU Langone Medical Center, identified a new player in TH17 cell differentiation, DEAD-box protein 5 (DDX5). DDX5 appears to selectively coordinate the transcription of TH17 genes that are required for inflammatory disorders, and works by recruiting and unwinding a long noncoding RNA (lncRNA), Rmrp.
Rastinejad adds, “These findings call for further investigation—the molecular aspects of how Rmrp participates in this process remain to be defined. Follow-up research could lead to even more potential drug targets for autoimmunity, which are highly needed since existing drugs don’t work for all patients.”
The full text of the paper is available here.