Multiple Sclerosis, 1 October 2002, vol. 8, no. 6, pp. 447-451(5)
Seifert T.[1]; Kieseier B.C.[1]; Ropele S.[2]; Strasser-Fuchs S.[1];
Quehenberger F.[3]; Fazekas F.[4]; Hartung H-P.[1]
[1] Department of Neurology, Karl Franzens University, Auenbruggerplatz
22, Graz A-8036, Austria [2] MRI Center, Karl Franzens University, Auenbruggerplatz
22, Graz A-8036, Austria [3] Institute for Medical Informatics, Statistics
and Documentation, Karl Franzens University, Engelgasse 13, Graz A-8010,
Austria [4] Department of Neurology, Karl Franzens University, Auenbruggerplatz
22, Graz A-8036, Austria and the MRI Center, Karl Franzens University,
Auenbruggerplatz 22, Graz A-8036, Austria
Tumor necrosis factor-a (TNF-a) is involved in the pathogenesis of multiple sclerosis (MS).
It has to be released from its cell membrane-bound precursor by proteolytic cleavage.
This is mainly performed by a member of the ADAM (a disintegrin and metalloproteinase) family of enzymes, TNF-a-converting enzyme (TACE, ADAM 17).
In a longitudinal study on 11 relapsing–remitting MS patients, we qualitatively determined mRNA expression of TNF-a and TACE in peripheral blood mononuclear cells (PBMCs) without ex vivo stimulation.
mRNA expression was related to disease activity as assessed by monthly gadolinium (Gd)-enhanced brain magnetic resonance imaging (MRI).
Patients found positive for TACE mRNA in PBMCs showed a significantly higher mean number of new Gd-enhancing lesions per scan one month following PBMC sampling.