Elevated Autoantibodies in Subacute Human Spinal Cord Injury Are Naturally Occurring Antibodies

Spinal cord injury (SCI) results in long-term neurological and systemic consequences, including antibody-mediated autoimmunity, which has been related to impaired functional recovery. Here we show that autoantibodies that increase at the subacute phase of human SCI, 1 month after lesion, are already...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in immunology Vol. 9; p. 2365
Main Authors Arevalo-Martin, Angel, Grassner, Lukas, Garcia-Ovejero, Daniel, Paniagua-Torija, Beatriz, Barroso-Garcia, Gemma, Arandilla, Alba G, Mach, Orpheus, Turrero, Angela, Vargas, Eduardo, Alcobendas, Monica, Rosell, Carmen, Alcaraz, Maria A, Ceruelo, Silvia, Casado, Rosa, Talavera, Francisco, Palazón, Ramiro, Sanchez-Blanco, Nuria, Maier, Doris, Esclarin, Ana, Molina-Holgado, Eduardo
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 11.10.2018
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Spinal cord injury (SCI) results in long-term neurological and systemic consequences, including antibody-mediated autoimmunity, which has been related to impaired functional recovery. Here we show that autoantibodies that increase at the subacute phase of human SCI, 1 month after lesion, are already present in healthy subjects and directed against non-native proteins rarely present in the normal spinal cord. The increase of these autoantibodies is a fast phenomenon-their levels are already elevated before 5 days after lesion-characteristic of secondary immune responses, further supporting their origin as natural antibodies. By proteomics studies we have identified that the increased autoantibodies are directed against 16 different nervous system and systemic self-antigens related to changes known to occur after SCI, including alterations in neural cell cytoskeleton, metabolism and bone remodeling. Overall, in the context of previous studies, our results offer an explanation to why autoimmunity develops after SCI and identify novel targets involved in SCI pathology that warrant further investigation.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Reviewed by: Irun R. Cohen, Weizmann Institute of Science, Israel; Hannelore Ehrenreich, Max-Planck-Institut für experimentelle Medizin, Germany
This article was submitted to Multiple Sclerosis and Neuroimmunology, a section of the journal Frontiers in Immunology
Edited by: Serge Nataf, Claude Bernard University Lyon 1, France
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2018.02365