New research at the University of Adelaide, Australia, may help pave the way toward the potential inhibition of multiple sclerosis (MS) and other autoimmune diseases. The study entitled “CCR2 defines in vivo development and homing of IL-23-driven GM-CSF-producing Th17 cells” was published in the journal Nature Communications. In the study, researchers showed that CCR2, a chemokine receptor, is involved in an exacerbated immune response that leads to the progression of MS and other autoimmune diseases.

MS is an untreatable neurodegenerative disease, affecting 23,000 individuals in Australia, and is considered the most frequent disease of the central nervous system (CNS) in young adults. MS has been described as an immune-mediated demyelinating condition, i.e. characterized by damage of the protective covering (myelin sheath) of nerve fibers in the brain and spinal cord.

The research team demonstrated that the chemokine receptor CCR2, and not CCR6, is a crucial inducer of encephalitogenic Th17 cell recruitment into the CNS, immune cells thought to be involved in MS pathogenesis. Thus, the team identified a distinctive cell surface signature and new developmental features of Th17 cells in vivo in the context of autoimmune encephalomyelitis (EAE), an experimental model for multiple sclerosis. This solved the important question regarding the molecular control of encephalitogenic Th17 cell migration to the CNS in EAE.

“Everybody has been focusing on the CCR6 receptor as the one to target to control this inflammatory response,” said senior author Professor Shaun McColl, Director of the Centre for Molecular Pathology at the University of Adelaide, in the press release. “We’ve now shown that the receptor to target is actually CCR2. Blocking CCR6 makes the disease worse. If we can find an antagonist to block the CCR2 receptor specifically on these T-cells, we should be able to control the progression of MS.” Professor McColl also emphasized that there is still no strategy available to control MS and there is an urgent need for the development of novel treatments for this condition.

The team believes that their research may also help improve the vaccine research field by contributing for improved vaccines to fight infection.

“Unlike in autoimmune diseases, where the body’s immune response is destroying its own cells and the aim is to block T-cell migration, with persistent infection we want to turn on the super-inflammatory response and enhance the migration of the immune cells to sites where they are needed,” explained Professor McColl.