Skip Navigation


International Immunology Advance Access originally published online on July 19, 2004
International Immunology 2004 16(9):1295-1304; doi:10.1093/intimm/dxh131
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
16/9/1295    most recent
dxh131v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (5)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Takasaki, Y.
Right arrow Articles by Hashimoto, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takasaki, Y.
Right arrow Articles by Hashimoto, H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© 2004 The Japanese Society for Immunology

Glyceraldehyde 3-phosphate dehydrogenase is a novel autoantigen leading autoimmune responses to proliferating cell nuclear antigen multiprotein complexes in lupus patients

Yoshinari Takasaki, Kazuhiko Kaneda, Masakazu Matsushita, Hirofumi Yamada, Masuyuki Nawata, Ran Matsudaira, Masanao Asano, Reiko Mineki1, Noriko Shindo1 and Hiroshi Hashimoto

Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine and 1 Division of Biochemical Analysis, Central Laboratory of Medical Science, Juntendo University School of Medicine, Tokyo 113-8421, Japan

Correspondence to: Y. Takasaki; E-mail: tyoshi{at}med.juntendo.ac.jp

Using 2-dimensional electrophoresis and ion-pair chromatography, we have identified elements of proliferating cell nuclear antigen (PCNA) multiprotein complexes that are reactive to antibodies in sera from patients with systemic lupus erythematosus. Among the various elements of the complexes, a 37 kDa protein (PI 8.5) that specifically reacted with SLE sera, but not with sera from patients with other connective tissue diseases, was identified as glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Immunoblot analysis showed that SLE sera reactive with the 37 kDa protein specifically reacted with GAPDH, as did anti-GAPDH mAbs. The purified autoantibodies to GAPDH from lupus serum showed both nuclear speckled and cytoplasmic staining patterns in immunofluorescence on Hep-2 cells. In addition, enzyme-linked immunosorbent assay (ELISA) revealed the presence of anti-GAPDH autoantibodies in 47% of lupus patients. Longitudinal analysis of the reactivity of lupus sera to PCNA complexes showed the autoimmune response to spread from GAPDH to other elements of PCNA complexes, and the presence of anti-GAPDH antibodies was significantly correlated with increased levels of serum PCNA. Taken together, these findings suggest that GAPDH interacting with PCNA in association with its cellular function is a novel autoantigen recognized by lupus sera, and that GAPDH thus plays an important role in the induction of autoimmune responses against the PCNA complex.

Keywords: antigens, autoantibodies, human, systemic lupus erythemtosus

Transmitting editor: K. Yamamoto


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Immunol.Home page
J. Kolln, H.-M. Ren, R.-R. Da, Y. Zhang, E. Spillner, M. Olek, N. Hermanowicz, L. G. Hilgenberg, M. A. Smith, S. van den Noort, et al.
Triosephosphate Isomerase- and Glyceraldehyde-3-Phosphate Dehydrogenase-Reactive Autoantibodies in the Cerebrospinal Fluid of Patients with Multiple Sclerosis
J. Immunol., October 15, 2006; 177(8): 5652 - 5658.
[Abstract] [Full Text] [PDF]

Home page
 LupusHome page
Y Xiang and T Kato
Use of Proteomics in Analysis of Autoimmune Diseases
Lupus, July 1, 2006; 15(7): 431 - 435.
[Abstract] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.