The cells in question, obtained from spinal fluid and blood samples, are called B cells, which normally help to clear foreign infections from the body but sometimes react strongly with the body itself. One of the current theories of multiple sclerosis, which strikes hundreds of thousands of Americans and millions more worldwide, holds that the disease manifests when self-reactive B cells in the brain become activated and cause inflammation there.
The apparent exchange of the cells between the brain and the blood may be a key to unlocking better treatments and diagnostics, because the activated B cells causing problems in the brain may be accessible when they move from the brain to the periphery.
"The hope is that if we can identify culprit B cells, using precise tools, we will be able to better diagnose multiple sclerosis and monitor disease activity. In addition, in ways that may have to be tailored for each patient, this may also allow us to develop therapies that directly target disease-causing B cells," said UCSF neurologist Hans Christian von Büdingen, MD, who led the research.
Described this week in the Journal of Clinical Investigation, the work is the latest from the UCSF Multiple Sclerosis Center, part of the UCSF Department of Neurology and one of the leading programs in multiple sclerosis research and patient care worldwide.
Since 2008, a UCSF team led by the chair of the Department of Neurology, Stephen Hauser, MD, has completed two clinical trials that showed, in essence, that blocking B cells may stop the attacks, or flare-ups, that occur in people with multiple sclerosis. These trials used Rituximab and Ocrelizumab, both of which target a molecule called CD20 found on the surface of B cells.
The new work suggests that targeting B cells could be extended into a precision strategy that would specifically tailor treatments to the exact identity of the B cells at work in any one patient.