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Compartmentalization of inflammation in the CNS: a major mechanism driving progressive multiple sclerosis

Edgar Meinl1, Markus Krumbholz, Tobias Derfuss

  • 1Department of Neuroimmunology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany. meinl@neuro.mpg.de

Journal of the Neurological Sciences
|August 22, 2008
PubMed

In multiple sclerosis (MS) the CNS is not only the target of the pathological immune response, but the CNS itself becomes an immunological compartment during the course of the disease. This comprises (i) inflammation beyond classical white matter lesions, (ii) intrathecal Ig production with oligoclonal bands, (iii) an environment fostering immune cell persistence, (iv) follicle-like aggregates in the meninges, (v) a disruption of the blood-brain barrier also outside of active lesions, which allows influx of autoantibodies possibly promoting demyelination or axonal injury and influx of fibrinogen driving inflammation.

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