The immune system balances the ability to fight off infectious invaders with the development of autoimmune diseases. One of the main players in this balancing act is a white blood cell known as a T cell.

A team from the UAB Department of Pathology has analyzed a subclass of T cells called Th1 cells and Th17 cells that make distinct products to attack different kinds of pathogens.

Until recently it was thought that these cells and their daughter cells did not differentiate or change, and only maintained an ability to make their unique combination of proteins.

UAB researchers have discovered that given certain environmental cues, Th17 cells no longer make their distinct proteins and begin to express the products Th1 cells make. 

Details of the mechanism that drives this "plasticity" were published May 28 in the journal Immunity.

"Th17 cells primarily make interleukin-17 (IL-17) among other proteins when exposed to extracellular bacteria and fungal pathogens," says UAB Assistant Professor Robin Hatton, Ph.D. "Under certain circumstances, Th17 cells can be diverted to become a Th1-like cell making interferon gamma and no longer expressing IL-17. Our findings form the basis of understanding the Th17 cell's ability to adapt in response to changing environmental cues."

By understanding how Th17 plasticity unfolds in normal and abnormal immunity, scientists hope to learn how to curb or harness the destructive potential of these cells as a way to find new treatments for autoimmune diseases, uncontrolled inflammation and cancer, said UAB Professor Casey Weaver, M.D., a co-author on the study.