Characterization of immune response in â-tubulin induced murine experimental autoimmune hearing loss (129.44)

• Published in: The Journal of immunology (1950) 2007-04, Vol.178 (1_Supplement), p.S226-S226
• Main Authors: Zhou, Bin, Glickstein, Jonathan, Zhou, Yixuan, Kermany, Mohammad Habiby, Cai, Chun, Cai, Qing, Kim, Jun Woo, Kim, Patrick, Liu, Wenxia, Yoo, Tai June
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.178.Supp.129.44

The pathological mechanism(s) of autoimmune sensorineural hearing loss (ASNHL) is still unknown. An autoimmune reaction to inner ear structures could be one of several possible pathogenic factors involved in ASNHL. In the current study we show that the inner ear–specific proteins b-tubulin are capable of targeting experimental autoimmune hearing loss (EAHL) in mice. Two weeks after immunization of BALB/c mice with b-tubulin, auditory brainstem responses (ABR) showed significant hearing loss, and the hearing loss can lasted at least six weeks. The antibodies activity to â-tubulin increased in dose dependent compared with controls. In addition, sera of these mice contained high levels of anti-â-tubulin antibodies could transferred EAHL to naive mice. Flow cytometry analysis showed that b-tubulin activated CD4+ T cells with a proinflammatory Th1-like phenotype. T cell mediation of EAHL was determined by showing significantly increased ABR thresholds 6 weeks after adoptive transfer of b-tubulin-activated CD4+ T cells into naive BALB/c recipients. Immunocytochemical analysis showed that leukocytic infiltration of inner ear tissues, and histological analysis showed that the loss of inner and outer hair cells in â-tubulin-immunized mice. Moreover, the percentage of CD4+CD25+ regulatory T cells and the level of FoxP3 were significantly decreased in EAHL. Our study provides an experimental confirmation that ASNHL may be a humoral and cellular immune reactivity against b-tubulin, which may be sufficient for mediating the hearing loss observed in ASNHL.