A molecular trio in relapse and remission in multiple sclerosis

Two thirds of patients with multiple sclerosis have the relapsing-remitting form, which often progresses to more debilitating disease. Striking clinical recovery, termed remission, often follows these periodic neurological defects, termed relapses. Recent work has revealed the role of three key molecules in relapse and remission: alpha 4 beta 1 integrin ( also known as VLA4) is an adhesion molecule that mediates T cell migration from the blood into the brain; osteopontin binds to alpha 4 beta 1 integrin, stimulating the production of pro-inflammatory cytokines and inhibiting apoptosis; and alpha B crystallin inhibits inflammation in the brain. This Review discusses how this molecular trio interacts to initiate relapses ( in the case of osteopontin and alpha 4 beta 1 integrin) and then to terminate them as remissions in multiple sclerosis (in the case of alpha B crystallin).