Table of Contents Author Guidelines Submit a Manuscript
Autoimmune Diseases
Volume 2015 (2015), Article ID 640171, 8 pages
Research Article

Hepatic but Not CNS-Expressed Human C-Reactive Protein Inhibits Experimental Autoimmune Encephalomyelitis in Transgenic Mice

1Department of Medicine, The University of Alabama Birmingham, Birmingham, AL 35294, USA
2Davis School of Gerontology and Department of Biological Sciences, The University of Southern California, Los Angeles, CA 90089, USA
3Department of Pathology, The University of Alabama Birmingham, Birmingham, AL 35294, USA

Received 9 July 2015; Accepted 13 August 2015

Academic Editor: Ricard Cervera

Copyright © 2015 Tyler T Wright et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We recently demonstrated that human C-reactive protein (CRP), expressed hepatically in transgenic mice (CRPtg), improved the outcome of experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). The liver is the primary site of CRP synthesis in humans and in CRPtg mice but is also expressed by both at low levels in the CNS. To determine if CNS expression of human CRP is sufficient to impact EAE, we generated neuronal CRP transgenic mice (nCRPtg) wherein human CRP expression is driven by the neuron-specific Ca2+/calmodulin-dependent protein kinase IIα (CaMKIIα) gene promoter. We found that hepatically expressed/blood-borne CRP, but not CNS expressed CRP, lessened EAE severity. These outcomes indicate that the protective actions of human CRP in EAE are manifested in the periphery and not in the CNS and reveal a previously unappreciated site specificity for the beneficial actions of CRP in CNS disease.