December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Fine and Finer Specificity of the TCCs Established from the Aqueous Humors of the VKH Disease Patients
Author Affiliations & Notes
  • K Yamaki
    Ophthalmology Akita Univ Sch of Med Akita Japan
  • Footnotes
    Commercial Relationships   K. Yamaki, None. Grant Identification: Grants-in-aid for scientific research from the Mnistry of Fundation, Science and Culuture of Japan.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1528. doi:
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      K Yamaki; Fine and Finer Specificity of the TCCs Established from the Aqueous Humors of the VKH Disease Patients . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1528.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose:Identification of the fine and finer specificity of the T cell clones (TCCs) reactive against tyrosinase family proteins established from the aqueous humors with Vogt-Koyanai-Harada disease (VKH) patients. Methods:The inflammatory cells in aqueous humors with VKH disease patients were collected in fresh and untreated stage. The cells were transformed with Herpes virus saimiri C488. The TCCs were generated by limiting dilution methods from transformed cells. Thus established TCCs were investigated their reactivity against tyrosianse and/or TRP1. The TCCs reactive against tyrosinase or TRP1 were further tested against about 30 mer amino acid (A.A) length peptides that cover entire tyrosianse or TRP1. Finer specificity was tested against 11mer A.A length peptides that covers the 30 mer A.A length peptides having the potential to proliferate the TCCs. Results:We reported that 6 and 4 clones from randomly selected 21 clones of TCCs were reactive to tyrosianse and TRP1, respectively. In this report, we tested fine (against 30 mer) and finer (against 11 mer) specificity of the clones that were reactive against tyrosinase. Four of the TCCs were reactive against the 30 mer peptides that have relatively strong binding site for HLA DRB1*0405. The finer specificity showed that these 4 TCCs were reactive against the strong binding sites of 11 mer peptides. The other 2 TCCs were reactive against different 30 mer peptides. Conclusion:Majority of the T cells infiltrating in aqueous humor with VKH disease were reactive to the strong binding sites for HLA DRB1*0405 of tyrosinase. It was suggested that T cells reactive against tyrosinase develop VKH disease.

Keywords: 327 autoimmune disease • 463 melanocytes • 612 uveitis-clinical/animal model 

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