A research team led by Francisco J. Quintana, PhD, Department of Neurology, has uncovered a mechanism behind which interleukin-27 influences dendritic cells’ control of T cell response in experimental autoimmune encephalomyelitis (EAE). The findings suggest that interleukin-27 signaling in dendritic cells limits pathogenic T cell responses and the development of autoimmunity.
Dendritic cells are a type of immune cell. One of their functions is to control the balance between effector and regulatory T helper cells (other forms of immune cells) with the help of a cell-signaling molecule called interleukin-27.
In pre-clinical models harboring interleukin-27 receptor-deficient dendritic cells, the researchers found that interleukin-27 signaling in the cells limited the creation of effector T helper cell 1 and T helper cell 17. The effects of interleukin-27 were regulated through ENTPD1 (CD39) gene expression in the dendritic cells. Moreover, vaccination with interleukin-27-conditioned dendritic cells suppressed established relapsing-remitting experimental autoimmune encephalomyelitis.
“Our studies identify a new mechanism by which interleukin-27 limits inflammation, and also describe a potential method for the exploitation of this immunoregulatory pathway for the treatment of autoimmune disorders,” said Quintana.
The study was published online Sept.1, 2013, in Nature Immunology.