Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Lunardi, C. et al.

Lunardi, Bason, Leandri, Navone, Lestani, Millo, Benatti, Cilli, Beri, Corrocher, Puccetti,

Autoantibodies to inner ear and endothelial antigens in Cogan's syndrome.

BACKGROUND: Cogan's syndrome is a chronic inflammatory disease of unknown origin, characterised by sensorineural hearing loss, episcleritis, and vasculitis. An autoimmune origin has been suggested but not proven. Our aim was to establish whether or not an autoimmune process is the cause of the disease. METHODS: We used pooled IgG immunoglobulins derived from eight patients with Cogan's syndrome to screen a random peptide library to identify disease relevant autoantigen peptides. Among the identified peptides, one was recognised by all the patients' sera. Antibodies against peptides were affinity purified from patients' sera and used to characterise the autoantigen, to stain human cochlea, and to transfer the features of Cogan's disease into animals. FINDINGS: We identified an immunodominant peptide that shows similarity with autoantigens such as SSA/Ro and with the reovirus III major core protein lambda 1. The peptide sequence shows similarity also with the cell-density enhanced protein tyrosine phosphatase-1 ( DEP-1/ CD148), which is expressed on the sensory epithelia of the inner ear and on endothelial cells. IgG antibodies against the peptide, purified from the patients' sera, recognised autoantigens and DEP-1/ CD148 protein, bound human cochlea, and inhibited proliferation of cells expressing DEP-1/ CD148. The same antibodies bound connexin 26, gene mutations of which lead to congenital inner-ear deafness. Furthermore, these antibodies were able to induce the features of Cogan's disease in mice. INTERPRETATION: Our results indicate that Cogan's syndrome is an autoimmune disease, characterised by the presence of autoantibodies able to induce tissue damage on binding of cell-surface molecules present on the sensory epithelia of the inner ear and on endothelial cells.[1]

References

Autoantibodies to inner ear and endothelial antigens in Cogan's syndrome. Lunardi, C., Bason, C., Leandri, M., Navone, R., Lestani, M., Millo, E., Benatti, U., Cilli, M., Beri, R., Corrocher, R., Puccetti, A. Lancet (2002) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.