St. Jude finds molecule that could improve cancer vaccines and therapy for othe...( Investigators at St. Jude Children's...),Health

Investigators at St. Jude Children's Research Hospital have discovered a new signaling molecule that prevents immune responses from running amok and damaging the body. The finding could lead to the development of new treatments for cancer, using vaccines; for autoimmune diseases, such as Type 1 diabetes; and for inflammatory diseases, such as inflammatory bowel disease (IBD) and asthma.

The St. Jude team discovered that specialized immune lymphocytes called regulatory T cells release a protein complex composed of two proteins called Ebi3 and Il12a. This protein complex acts like a brake on the activity of the aggressive immune cells called effector T lymphocytes. A report on this discovery appears in the journal Nature Nov. 22, 2007.

The newly recognized protein complex is one of a large group of signaling molecules called cytokines that cells use to communicate with each other. Since the immune system cytokines are called interleukins, the St. Jude team named this protein interleukin-35 (IL-35). Most cytokines stimulate immune system cells by driving the immune attack or causing inflammation. However, IL-35 is one of the few signaling molecules known to inhibit immune system activity.

The discovery of IL-35 is important because the manipulation of regulatory T cells is a key goal of immunotherapy, said Dario Vignali, Ph.D., associate member in the St. Jude Department of Immunology, and the papers senior author. Immunotherapy is the treatment of infections, cancer or other diseases by manipulating the immune system to enhance or restrict its activity. Despite the fact that regulatory T cell-mediated immunotherapy holds promise for patients, the molecules responsible for the cells ability to suppress immune system activity are largely unknown, a problem that has slowed progress in this field.

The St. Jude team showed that the genes that produce IL-35 (Ebi3 and II12a) are active in regulatory T cells but not in effector T ce
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