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Study: Accumulation of B cells triggers nervous system damage in MS
November 14, 2018
B cells are important in helping the immune system fight pathogens. However, in the case of multiple sclerosis they can damage nerve tissue. When particular control cells are missing, too many B cells accumulate in the meninges, resulting in inflammation of the central nervous system. Technical University of Munich researchers demonstrated the process using a mouse model of MS and patient samples.
Myeloid-derived suppressor cells (MDSCs) function as an important control mechanism in the immune system and make sure that immunoreactions do not become too strong. In the case of MS these controls in the nervous system appear to fail in part. Using a mouse model of MS, researchers removed the MDSCs from the meningeal tissue and then observed an increase in the accumulation of B cells there. At the same time inflammation and damage occurred, triggered by the high number of B cells in the nerve tissue. This phenomenon did not occur when enough MDSCs were present, controlling the number of B cells.
Based on 25 tests of the cerebrospinal fluid of subjects with MS, the lack of MDSCs could also have a negative effect on the course of the illness in patients. When the researchers found large numbers of MDSCs in CSF, the patients usually also experienced milder symptoms with fewer episodes of inflammation. In contrast, patients with lower MDSC counts experienced stronger symptoms. Because the number of subjects tested in this case was small, researchers are planning larger patient studies for the future.
In the future, the researchers want to explain how the B cells destroy the nervous system. According to the authors there are two possibilities: In the meninges B cells emit substances that attract immune cells that then incorrectly destroy the body's own tissues; or, B cells activate immune cells in the blood and lymph systems which then move to the meninges, where they cause damage
The findings were published in the journal
Nature Immunology
.
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