In separate studies, Nico Ghilardi of Genentech Inc. (NYSE:DNA) in San Francisco and Christopher Hunter of the University of Pennsylvania studied different mouse models of brain inflammation that resemble human diseases, such as multiple sclerosis.

Both studies show brain inflammation is worse in mice that cannot respond to interleukin 27, a factor that communicates messages to immune cells. Such increased brain inflammation is associated with an influx of T cells that produce a molecule known to promote inflammation -- interleukin 17 -- into the brain.

The researchers found treatment of T cells with interleukin 27 blocks the development of cells that produce interleukin 17.

Therefore, the scientists posit preventing harmful interleukin 17-producing cells from developing, interleukin 27 could represent a potential therapeutic target for treating autoimmune diseases.

The study appears in the journal Nature Immunology.