alexa Antibodies to an Intracellular Antigen Penetrate Neuronal Cells and Cause Deleterious Effects
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
Open Access

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Research Article

Antibodies to an Intracellular Antigen Penetrate Neuronal Cells and Cause Deleterious Effects

Joshua N Douglas1,2#, Lidia A Gardner1,2# and Michael C Levin1,2*
1Department of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, USA
2Research Service VA Medical Center, Memphis, TN, 38104, USA
#Authors contributed equally
Corresponding Author : Michael C. Levin
Department of Neurology
University of TN Health Science Center, 855 Monroe Avenue
Room 415, Memphis, TN, 38163, USA.
Tel: 901-523-8990 (Ext. 6809)
Fax: 901-577-7273
E-mail: [email protected]
Received November 29, 2012; Accepted January 24, 2013; Published January 30, 2013
Citation: Douglas JN, Gardner LA, Levin MC (2013) Antibodies to an Intracellular Antigen Penetrate Neuronal Cells and Cause Deleterious Effects. J Clin Cell Immunol 4:134. doi:10.4172/2155-9899.1000134
Copyright: © 2013 Douglas JN, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Multiple sclerosis (MS) is an autoimmune disease that is increasingly being recognized as a neurodegenerative disorder. Patients with MS produce autoantibodies to heterogenous nuclear ribonucleoprotein A1 (hnRNPA1). A multitude of studies indicate that T-lymphocytes, B-lymphocytes and macrophages contribute to MS pathogenesis. However, a direct autoantibody impact on neuronal cells has received limited attention. This could be explained by the general belief that autoantibodies lack the ability to penetrate neurons. hnRNP A1 is an intracellular RNA binding protein that exports RNA from the nucleus to the cytoplasm. In this study, we investigated possible mechanisms of antibody penetration into neuronal cells. Our results show that anti-hnRNP A1 antibodies and control IgG penetrate SK-N-SH neuronal cells through clathrin-mediated endocytosis. In contrast to control antibodies, anti-hnRNP A1 antibodies produced deleterious effects on the neuronal cells including altered ATP levels and increased caspase 3/7 levels (leading to apoptosis). Remarkably, anti-hnRNP A1 antibodies that targeted the hnRNP A1 M9 domain (its nuclear export/localization sequence) caused redistribution of endogenous hnRNPA1 protein in neuronal cells. These findings indicate that anti-hnRNPA1 antibodies might contribute to the pathogenesis of MS.

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