edoc

Natalizumab alters transcriptional expression profiles of blood cell subpopulations of multiple sclerosis patients

Lindberg, R. L. and Achtnichts, L. and Hoffmann, F. and Kuhle, J. and Kappos, L.. (2008) Natalizumab alters transcriptional expression profiles of blood cell subpopulations of multiple sclerosis patients. Journal of neuroimmunology, Vol. 194. pp. 153-164.

Full text not available from this repository.

Official URL: http://edoc.unibas.ch/dok/A6004986

Downloads: Statistics Overview

Abstract

Natalizumab, the most recently approved treatment for relapsing multiple sclerosis (MS) exerts its action through binding to alpha4 integrins. We studied longitudinally gene expression profiles in peripheral blood of MS patients, treated with natalizumab for more than 2 years. The majority of altered genes relates to immune response, signal transduction, adhesion and metabolism. Not only gene expression relevant for T lymphocytes was altered, but also genes regulating B-lymphocyte, neutrophil and erythrocyte functions. Understanding these different gene effects and their interrelationships will provide more insights into additional mechanisms of action of natalizumab and possibly allow better prediction of adverse events.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Clinical Neuroimmunology (Derfuss/Lindberg)
03 Faculty of Medicine > Bereich Medizinische Fächer (Klinik) > Neurologie > Neuroimmunologie (Kappos)
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Medizinische Fächer (Klinik) > Neurologie > Neuroimmunologie (Kappos)
UniBasel Contributors:Kappos, Ludwig and Lindberg Gasser, Raija L.P.
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Elsevier
ISSN:0165-5728
Note:Publication type according to Uni Basel Research Database: Journal article
Related URLs:
Identification Number:
Last Modified:07 Dec 2012 13:03
Deposited On:07 Dec 2012 13:00

Repository Staff Only: item control page