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Scientific Commentary |
T cells and microglia as drivers of multiple sclerosis pathology
| The first 10% of the full text of this article appears below. |
One of the many open questions in multiple sclerosis research is whether inflammation in the CNS is initiated by an autoimmune attack, triggered by unidentified environmental factors, or represents a response to axonal degeneration and myelin degradation secondary to processes that are intrinsic to the CNS.
The autoimmune hypothesis is supported by the recently well-established disease association with genes in the HLA region which encode proteins that are functionally relevant for initiating immune responses by presenting peptides to CD4+ and CD8+ T cells (Lincoln et al., 2005
; Oksenberg et al., 2004). Functional evidence was provided initially by the animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), which showed that the minimal requirement to trigger disease is activated T cells (Ben-Nun et al., 1981
Department of Clinical Neurology and MRC Human
Immunology Unit
Weatherall Institute of Molecular Medicine
John Radcliffe Hospital
University of Oxford
Oxford OX3 9DS
UK
E-mail: Lars.fugger@imm.ox.ac.uk