期刊
JOURNAL OF MOLECULAR MEDICINE-JMM
卷 88, 期 8, 页码 753-761出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00109-010-0632-3
关键词
Multiple sclerosis; Neurofascin; Contactin-2; Grey matter injury; Cortical lesions; Node of Ranvier
资金
- Deutsche Forschungsgemeinschaft [SFB 571]
- Verein zur Therapieforschung fur Multiple Sklerose-Kranke
- BMBF (krankheitsbezogenes Kompetenznetz Multiple Sklerose) [Forderkennzeichen 01GI0905]
- Excellency Initiative of the Ludwig-Maximilian-University Munich
Multiple sclerosis is thought to be an autoimmune-mediated disease of the central nervous system. For many years, T-cells were regarded as the key players in the pathogenesis, and myelin of white matter was considered as the main victim. However, research during recent years showed a more complex picture. Besides T-cells, also B-cells, antibodies and the innate immunity contribute to the tissue damage. Modern imaging techniques and neuropathological examinations showed that not only myelin but also axons, cortical neurons and nodes of Ranvier are damaged. The autoimmune targets of this widespread injury are so far not known. The identification of the axo-glial proteins contactin-2 and neurofascin provides excellent examples how antibodies can induce axonal injury at the node of Ranvier and how T-cells can destruct cortical integrity. This review will discuss the pathogenic implications of an autoimmune response against these newly discovered antigens.
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