CD6 as a potential target for treating multiple sclerosis

Significance Multiple sclerosis (MS), an autoimmune disease that affects the central nervous system, is driven by activated T lymphocytes that invade the brain and spinal cord, leading to damage to the myelin sheaths that surround nerve axons. Current treatments are only partly successful, especially for the later stages of chronic forms of MS. Experimental autoimmune encephalomyelitis (EAE) is a useful animal model of MS, suitable for testing new approaches to treatment. By genetically altering mice to eliminate a T lymphocyte surface protein known as CD6, we show that the CD6 molecule is essential for the development of EAE. Furthermore, an anti-CD6 monoclonal antibody is effective in treating EAE in mice that express human CD6 but not mouse CD6 on their T lymphocytes.