Preprint Article Version 1 This version is not peer-reviewed

TGF-Beta 1 and the Spinal Cord-Specific Outcome of Multiple Sclerosis Active Plaques

Version 1 : Received: 13 December 2017 / Approved: 20 December 2017 / Online: 20 December 2017 (07:04:10 CET)

How to cite: Nataf, S. TGF-Beta 1 and the Spinal Cord-Specific Outcome of Multiple Sclerosis Active Plaques. Preprints 2017, 2017120138 (doi: 10.20944/preprints201712.0138.v1). Nataf, S. TGF-Beta 1 and the Spinal Cord-Specific Outcome of Multiple Sclerosis Active Plaques. Preprints 2017, 2017120138 (doi: 10.20944/preprints201712.0138.v1).

Abstract

We recently reported that in the spinal cord of PPMS or SPMS patients, large areas of periplaque demyelinating lesions extend distance away from plaque borders. Such lesions are characterized by a progliotic TGF-beta 1 signature accompanied by: i) a low-grade inflammatory reaction, ii) an extensive astrocytosis and iii) a process of incomplete demyelination. It was proposed that, while efficiently dampening inflammation in MS spinal cords, TGF-beta 1 could promote astrocytosis, prevent remyelination and possibly trigger alterations of myelin synthesis. In light of these findings, a re-interpretation of two large neuropathological studies performed on MS brains and spinal cords is provided here. While results from these studies clearly showed that active plaques do not display any region-specific distribution, an important point was apparently overlooked and not discussed by the authors: a significantly higher percentage of inactive plaques was found in MS spinal cords as compared to brains and, conversely, the percentage of slowly-expanding (or smoldering) lesions was significantly lower in the spinal cord as compared to the brain. These data indicate that the spinal cord environment may be more favorable to the resolution of inflammation. Downstream of the autoimmune process leading to plaque formation, region-specific mechanisms may thus drive the outcome of active plaques. While inflammation triggers tissue destruction, inflammation may also be needed for effective tissue repair and an inappropriate dampening of inflammatory events may possibly translate into a poor level of remyelination in MS spinal cords. It is proposed here that TGF-beta 1 is involved in such a brain-spinal cord dissociation of active plaques outcome.

Subject Areas

multiple sclerosis; spinal cord; transforming growth factor beta 1; active plaques

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