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More MS news articles for February 2004

Deficient p75 low-affinity neurotrophin receptor expression exacerbates experimental allergic encephalomyelitis in C57/BL6 mice

J Neuroimmunol. 2004 Mar;148(1-2):41-53
Copray S, Kust B, Emmer B, Young Lin M, Liem R, Amor S, De Vries H, Floris S, Boddeke E.
Department of Medical Physiology, University of Groningen, A.Deusinglaan 1, 9713 AV Groningen KZ, Netherlands.

We have investigated the role of p75(NTR) in inflammation in experimental allergic encephalomyelitis (EAE), a model for the human disease multiple sclerosis (MS).

Induction of EAE in C57/BL6 wild-type mice resulted in expression of p75(NTR) in endothelial cells in the CNS.

In contrast to the clinical manifestation of EAE observed in wild-type C57/BL6 mice, mice deficient for p75(NTR) (p75(NTR) knockout mice) developed severe or lethal disease and concomitant increased levels of inflammation in the CNS.

Our findings suggest a physiological significant role for p75(NTR) in CNS endothelial cells during inflammation and involvement in preservation of blood-brain barrier integrity during a severe infiltrative attack.