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Published in the journal Nature Communications, the researchers at the University of Adelaide have identified a key protein involved in a super-inflammatory immune response that drives the progression of multiple sclerosis and other autoimmune diseases.

The protein is a specific chemokine receptor involved in moving the body's immune response cells, the T-cells, around the body when they are in the super-inflammatory mode needed to fight persistent infections or conversely, as in the case of autoimmune diseases like multiple sclerosis, attacking the body's own tissues.
This chemokine receptor, called CCR2, is a different receptor than was widely assumed to be involved.

Researchers 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 multiple sclerosis pathogenesis. Thus, researchers 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 autoimmune encephalomyelitis. ( Xagena )

Source: University of Adelaide, 2015

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