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Role of alpha-metylacyl-CoA racemase in immune cells during the development of experimental autoimmune encephalomyelitis

 
: Tafferner, N.; Männich, J.; Eberle, M.; Ferreiros, N.; Debruin, N.; Geisslinger, G.; Parnham, M.J.; Schiffmann, S.

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Journal of neuroimmunology 275 (2014), No.1-2, pp.121–122
ISSN: 0165-5728
English
Journal Article
Fraunhofer IME ()

Abstract
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system and alteration of the metabolism of immune cells is an attractive strategy to modify their function during autoimmunity in MS. We investigated the effect of modulating fatty acid metabolism in an animal model of multiple sclerosis, myelin oligodendrocyte glycoprotein (MOG)35–55-induced, chronic progressive, experimental autoimmune encephalomyelitis (EAE) in C57/BL6 mice. Alpha-methylacyl-CoA racemase (AMACR) converts R-configurated branched fatty acids to the S-configuration, thereby preparing them for metabolic β-oxidation. We observed significant, selective, disease-dependent elevation of AMACR expression in various immune cells (monocytes/B cells/T cells) isolated from blood, draining lymph nodes and spleen in EAE mice during the preclinical phase. In vitro studies revealed that genetic deletion of AMACR inhibits the proliferation of T cells. However, AMACR−/− mice showed only a slight worsening of early (days 12–14) clinical symptoms of EAE and no alteration in cognitive behavior in comparison to wild type mice. This was accompanied over the same period by an increased number of neutrophils in the blood and of B cells and T cells in the lymph nodes of AMACR−/− EAE mice in comparison to wild-type EAE mice. In conclusion, our data suggest that AMACR is regulated in immune cells during EAE but it is not essential for the development of EAE.

: http://publica.fraunhofer.de/documents/N-439206.html