A molecular switch that limits the cells that cause autoimmune diseases

The immune system of human beings contains a specific subtype of white blood cells called “T helper 17” cells (TH17) which protect our organism from bacterial and fungal infections. But sometimes they get out of control, causing chronic inflammation and exposing us to the risk of autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, and Crohn’s disease.

In a study published in Nature Immunology, the research team led by Prof. Federica Sallusto (IRB, affiliated to USI Università della Svizzera italiana) has discovered that not all TH17 cells behave the same upon activation and there are indeed two subsets of human TH17 cells: one “good” that can help fighting the infections and keep the immune response under control, and one “bad” that can be also necessary to kill the pathogens, but could in some cases induce chronic inflammation, tissue damage and promote autoimmune diseases. The "good" TH17 cells are distinguished by their ability to activate a molecular "switch" that induces cytokines, small proteins important for cell communications, that quench inflammation and other important molecules to enhance tissue repair.

The next step in the work of Prof. Sallusto and her colleagues will be to identify how to transform the “bad” subset of TH17 cells into the ‘good’ one, which could eventually lead to new therapies against autoimmune and inflammatory diseases. 

For full details on the study entitled “An immunoregulatory and tissue-residency program modulated by c-MAF in human TH17 cells”:
www.nature.com/articles/s41590-018-0200-5