Cross-reaction between tyrosinase peptides and cytomegalovirus antigen by T cells from patients with Vogt-Koyanagi-Harada disease

被引：68

作者：

Sugita S. ^{[1
]}

Takase H. ^{[1
]}

Kawaguchi T. ^{[1
]}

Taguchi C. ^{[2
]}

Mochizuki M. ^{[1
]}

机构：

[1] Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8519

[2] Department of Ophthalmology, Kurume University School of Medicine, Kurume, Fukuoka

来源：

International Ophthalmology | 2007年 / 27卷 / 2-3期

关键词：

Autoimmune disease; Cross-reaction; Melanocyte; T cells; Virusantigens;

D O I：

10.1007/s10792-006-9020-y

中图分类号：

学科分类号：

摘要：

Aim: To determine whether T lymphocytes of patients with Vogt-Koyanagi-Harada (VKH) disease cross-react with peptides of melanocytes and with exogenous antigens. Methods: Cross-reactivity with melanocyte peptides, tyrosinase (tyrosinase450-462: SYLQDSDPDSFQD) and the mimic virus peptide, i.e., cytomegalovirus envelope glycoprotein H (CMV-egH290-302: SYLKDSDFLDAAL) was examined by a lymphocyte proliferation assay or cytokine production. The seroprevalence of various viruses was examined by a complement fixation test. To examine if the virus infections in VKH patients were latent, we measured genomic DNA of the virus using real-time polymerase chain reaction (PCR). Result: Some of the T cells established from VKH recognized melanocyte peptides including the tyrosinase peptide as well as the CMV-egH290-302 peptide, which had a high amino acid homology to the tyrosinase peptide. Cytomegalovirus (CMV) peptide-specific T cells showed a significant proliferation not only to CMV-egH290-302 but also to tyrosinase450-462. The seroprevalence of CMV was significantly higher in VKH patients. In addition, all tested samples of VKH patients were negative for CMV-DNA. Conclusions: These results indicate that CMV infection may stimulate the production of T cells that cross-react with tyrosinase by a mechanism of molecular mimicry. These events may be responsible for the onset of VKH disease. © Springer Science+Business Media, Inc. 2007.

引用

页码：87 / 95

页数：8

共 24 条

[1]

Lubin J.R., Ni C., Albert D.M., Clinicopathological study of the Vogt-Koyanagi-Harada syndrome, Int Ophthalmol Clin, 22, pp. 141-146, (1982)

[2]

Shindo Y., Inoko H., Yamamoto T., Et al., HLA-DRB1 typing of Vogt-Koyanagi-Harada's disease by PCR-RFLP and the strong association with DRB1*0405 and DRB1*0410, Br J Ophthalmol, 78, pp. 223-226, (1994)

[3]

Hammer H., Cellular hypersensitivity to uveal pigment confirmed by leukocyte migration tests in sympathetic ophthalmia and the Vogt-Koyanagi-Harada syndrome, Br J Ophthalmol, 58, pp. 773-776, (1974)

[4]

Read R.W., Rao N.A., Cunningham E.T., Vogt-Koyanagi-Harada disease, Curr Opin Ophthalmol, 11, pp. 437-442, (2000)

[5]

Kaplan M.H., Meyeserian M., An immunological cross-reaction between group A streptococcal cells and human heart tissue, Lancet, 1, pp. 706-710, (1962)

[6]

Michael B., Oldstone A., Molecular mimicry and autoimmune disease, Cell, 50, pp. 819-820, (1987)

[7]

Fujinami R.S., Oldstone M.B.A., Amino acid homology and immune response between the encephalitogenic site of myelin basic protein and virus: A mechanism for autoimmunity, Science, 230, pp. 1043-1045, (1985)

[8]

Ferrari I., Levin M.J., Wallkat G., Et al., Molecular mimicry between the immunodominant ribosomal protein PO of Trypanosoma crusi and a functional epitope on the human b1-adrenergic receptor, J Exp Med, 182, pp. 59-65, (1995)

[9]

Shimoda S., Nakamura M., Ishibash H., Et al., HLA DRB4 0101-restricted immunodominant T cell autoepitope of pyruvate dehydrogenase complex in primary biliary cirrhosis: Evidence of molecular mimicry in human autoimmune diseases, J Exp Med, 181, pp. 1835-1845, (1995)

[10]

Albani S., Carson D., A multistep molecular mimicry hypothesis for the pathogenesis of rheumatoid arthritis, Immunol Today, 17, pp. 466-470, (1996)

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