Myb regulates the function of regulatory T cells

Described in the journal Immunity, a study of the University of Melbourne reveals that the transcription factor Myb modulates the function of a subtype of immune cells, called regulatory T (Treg) cells.

Treg cells maintain immune homeostasis by limiting autoimmune and inflammatory responses. Understanding how the function of Treg cells is modulated would have profound implications. These cells often express CD4, CD25, IL-2 receptor alpha, and other Treg related molecules. In addition, a transcription factor called Foxp3 is the master regulator for the differentiation, maintenance, and function of Treg cells.

Activated Treg cells undergo further differentiation into an effector state that highly expresses genes crucial for Treg cell function. Until now, the mechanism underlying this process remains largely unknown.

In this study, lead researcher Stephen Nutt and colleagues found that the lack of Myb in Treg cells caused mice to succumb to an inflammatory disease. Further investigation showed that Myb was essential for the differentiation of thymus-derived effector Treg cells and that Myb regulated the expression of many genes specific to effector Treg cells. Collectively, the data suggest that the transcription factor Myb is very important for effector Treg cell differentiation and function.

The Myb gene is considered to be an oncogene. Scientists have known for many years that Myb is implicated in tumorigenesis. This study is the first to show that Myb plays a vital role in the immune system, according to the first author of the study, Sheila Dias.

Treg cells suppress immune responses, preventing the immune system from overacting to a threat. The study revealed that without the influence of Myb, Treg cells would allow the immune response to go out of control and cause severe inflammation. Thus, manipulating the action of Myb might be a way to control the immune response.
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