Johns Hopkins researchers discover key protein linked to transverse myelitis and multiple sclerosis

Hopkins researchers have discovered a single molecule that is a cause of an autoimmune disease in the central nervous system, called transverse myelitis (TM), that is related to multiple sclerosis.

In a study published in the October issue of The Journal of Clinical Investigation, psychiatrist Adam Kaplin, M.D., Ph.D., an assistant professor at The Johns Hopkins University School of Medicine, and neurologist Douglas Kerr, M.D., Ph.D., also an assistant professor at Hopkins, showed that the levels of the protein, IL-6, are dramatically elevated in the spinal fluid of transverse myelitis (TM) patients.

Although the majority of TM patients suffer a single attack, 15 percent to 30 percent of patients go on to develop full-blown MS. TM evolves rapidly and without warning and usually results in permanent impairment, including weakness of the legs and arms, bowel and bladder dysfunction, pain and paralysis.

IL-6 is a chemical messenger that cells of the immune system use to communicate with one another. One of the cell types injured by high levels of IL-6 includes oligodendrocytes, which help produce the protective myelin sheath coating around nerve cells. The findings offer one possible mechanism responsible for demyelinating disorders, such as TM and MS, and may aid in the development of effective therapies against these disorders, the researchers say.

"This is the first time a single culprit has been identified as causing a CNS autoimmune disease," said Kaplin.

The researchers began investigating the protein IL-6 when they became aware that TM patients suffered from memory impairment and depression. IL-6 has been implicated in mood and concentration disorders.

"This discovery is a success story that begins with listening carefully to what patients are telling us about their suffering and then collaborating across disciplines to open up new avenues of investigation," said Kaplin.

"TM is related to other autoimmune

Contact: Eric Vohr
Johns Hopkins Medical Institutions

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