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Science  11 Mar 2005:
Vol. 307, Issue 5715, pp. 1535-1537
DOI: 10.1126/science.307.5715.1535e

In the autoimmune condition multiple sclerosis, demyelination and axonal damage ultimately result in impaired motor function. The disease is thought to be caused by invading T cells that react against self components of the central nervous system (CNS), although the identity and location of antigen-presenting cells (APCs) that activate pathogenic T cells is a matter of speculation.

Greter et al. studied a multiple sclerosis system in which T cells reactive to a myelin antigen induce experimental autoimmune encephalomyelitis (EAE) upon transfer to mice. Animals lacking organized central lymphoid tissue developed EAE as quickly and with the same severity as control animals, suggesting that pathogenic T cells do not need to be reactivated in peripheral lymphoid organs in order to migrate to the CNS. Resident APCs of the CNS—microglial cells and astrocytes—did not appear to be important for causing disease. Instead, a subset of nonresident dendritic cells was required for disease to progress. In the model and in multiple sclerosis lesions, similar dendritic cells were associated with microvessels of the CNS, suggesting that activation and entry of autoreactive T cells may occur through the presentation of antigen at the blood-brain barrier. — SJS

Nature Med. 11, 328 (2005).

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