| Literature DB >> 21145286 |
Bin Zhou1, Mohammad Habiby Kermany, Jonathan Glickstein, Qing Cai, Chun Cai, Yixuan Zhou, Usha Nair, Jun Woo Kim, Patrick Kim, Wenxia Liu, Siva Kanangat, Tai June Yoo.
Abstract
Autoimmune inner ear disease is described as progressive, bilateral although asymmetric, sensorineural hearing loss and can be improved by immunosuppressive therapy. We showed that the inner ear autoantigen β-tubulin is capable of inducing experimental autoimmune hearing loss (EAHL) in mice. Immunization of BALB/c mice with β-tubulin resulted in hair cell loss and hearing loss, effects that were not seen in animals immunized with control peptide. Moreover, the EAHL model showed that β-tubulin responsiveness involved CD4(+) T cells producing IFN-γ, and T cell mediation of EAHL was determined by significantly increased auditory brainstem response after adoptive transfer of β-tubulin-activated CD4(+) T cells into naive BALB/c recipients. The potential mechanisms responsible for the observed pathology of EAHL can be attributed to decreased frequency and impaired suppressive function of regulatory T cells. Our study suggests that EAHL may be a T cell-mediated organ-specific autoimmune disorder of the inner ear. Published by Elsevier Inc.Entities:
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Year: 2010 PMID: 21145286 DOI: 10.1016/j.clim.2010.11.007
Source DB: PubMed Journal: Clin Immunol ISSN: 1521-6616 Impact factor: 3.969