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Erschienen in: International Ophthalmology 2-3/2007

01.06.2007 | Original Paper

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

verfasst von: Sunao Sugita, Hiroshi Takase, Tatsushi Kawaguchi, Chikako Taguchi, Manabu Mochizuki

Erschienen in: International Ophthalmology | Ausgabe 2-3/2007

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Abstract

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.
Literatur
1.
Zurück zum Zitat Lubin JR, Ni C, Albert DM (1982) Clinicopathological study of the Vogt–Koyanagi–Harada syndrome. Int Ophthalmol Clin 22:141–146PubMedCrossRef Lubin JR, Ni C, Albert DM (1982) Clinicopathological study of the Vogt–Koyanagi–Harada syndrome. Int Ophthalmol Clin 22:141–146PubMedCrossRef
2.
Zurück zum Zitat Shindo Y, Inoko H, Yamamoto T, et al (1994) 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 78:223–226PubMed Shindo Y, Inoko H, Yamamoto T, et al (1994) 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 78:223–226PubMed
3.
Zurück zum Zitat Hammer H (1974) Cellular hypersensitivity to uveal pigment confirmed by leukocyte migration tests in sympathetic ophthalmia and the Vogt–Koyanagi–Harada syndrome. Br J Ophthalmol 58:773–776PubMed Hammer H (1974) Cellular hypersensitivity to uveal pigment confirmed by leukocyte migration tests in sympathetic ophthalmia and the Vogt–Koyanagi–Harada syndrome. Br J Ophthalmol 58:773–776PubMed
4.
Zurück zum Zitat Read RW, Rao NA, Cunningham ET (2000) Vogt–Koyanagi–Harada disease. Curr Opin Ophthalmol 11:437–442PubMedCrossRef Read RW, Rao NA, Cunningham ET (2000) Vogt–Koyanagi–Harada disease. Curr Opin Ophthalmol 11:437–442PubMedCrossRef
5.
Zurück zum Zitat Kaplan MH, Meyeserian M (1962) An immunological cross-reaction between group A streptococcal cells and human heart tissue. Lancet 1:706–710PubMedCrossRef Kaplan MH, Meyeserian M (1962) An immunological cross-reaction between group A streptococcal cells and human heart tissue. Lancet 1:706–710PubMedCrossRef
6.
Zurück zum Zitat Michael B, Oldstone A (1987) Molecular mimicry and autoimmune disease. Cell 50:819–820CrossRef Michael B, Oldstone A (1987) Molecular mimicry and autoimmune disease. Cell 50:819–820CrossRef
7.
Zurück zum Zitat Fujinami RS, Oldstone MBA (1985) Amino acid homology and immune response between the encephalitogenic site of myelin basic protein and virus: a mechanism for autoimmunity. Science 230:1043–1045PubMedCrossRef Fujinami RS, Oldstone MBA (1985) Amino acid homology and immune response between the encephalitogenic site of myelin basic protein and virus: a mechanism for autoimmunity. Science 230:1043–1045PubMedCrossRef
8.
Zurück zum Zitat Ferrari I, Levin MJ, Wallkat G, et al (1995) Molecular mimicry between the immunodominant ribosomal protein PO of Trypanosoma crusi and a functional epitope on the human b1-adrenergic receptor. J Exp Med 182:59–65PubMedCrossRef Ferrari I, Levin MJ, Wallkat G, et al (1995) Molecular mimicry between the immunodominant ribosomal protein PO of Trypanosoma crusi and a functional epitope on the human b1-adrenergic receptor. J Exp Med 182:59–65PubMedCrossRef
9.
Zurück zum Zitat Shimoda S, Nakamura M, Ishibash H, et al (1995) 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 181:1835–1845PubMedCrossRef Shimoda S, Nakamura M, Ishibash H, et al (1995) 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 181:1835–1845PubMedCrossRef
10.
Zurück zum Zitat Albani S, Carson D (1996) A multistep molecular mimicry hypothesis for the pathogenesis of rheumatoid arthritis. Immunol Today 17:466–470PubMedCrossRef Albani S, Carson D (1996) A multistep molecular mimicry hypothesis for the pathogenesis of rheumatoid arthritis. Immunol Today 17:466–470PubMedCrossRef
11.
Zurück zum Zitat Zhao Z, Granucci S, Yeh F, et al (1998) Molecular mimicry by herpes simplex virus-type 1: autoimmune disease after viral infection. Science 279:1344–1353PubMedCrossRef Zhao Z, Granucci S, Yeh F, et al (1998) Molecular mimicry by herpes simplex virus-type 1: autoimmune disease after viral infection. Science 279:1344–1353PubMedCrossRef
12.
Zurück zum Zitat Bassili SS, Peyman GA, Gebhardt BM, et al (1996) Detection of Epstein–Barr virus DNA by polymerase chain reaction in the vitreous from a patient with Vogt–Koyanagi–Harada syndrome. Retina 16:160–161PubMedCrossRef Bassili SS, Peyman GA, Gebhardt BM, et al (1996) Detection of Epstein–Barr virus DNA by polymerase chain reaction in the vitreous from a patient with Vogt–Koyanagi–Harada syndrome. Retina 16:160–161PubMedCrossRef
13.
Zurück zum Zitat Sugita S, Takase H, Taguchi C, et al (2006) Ocular infiltrating CD4+ T cells from patients with Vogt–Koyanagi–Harada disease recognize human melanocyte antigens. Invest Ophthalmol Vis Sci 47:2547–2554PubMedCrossRef Sugita S, Takase H, Taguchi C, et al (2006) Ocular infiltrating CD4+ T cells from patients with Vogt–Koyanagi–Harada disease recognize human melanocyte antigens. Invest Ophthalmol Vis Sci 47:2547–2554PubMedCrossRef
14.
Zurück zum Zitat Read RW, Holland GN, Rao NA, et al (2001) Revised diagnostic criteria for Vogt–Koyanagi–Harada disease: report of an international committee on nomenclature. Am J Ophthalmol 131:647–652PubMedCrossRef Read RW, Holland GN, Rao NA, et al (2001) Revised diagnostic criteria for Vogt–Koyanagi–Harada disease: report of an international committee on nomenclature. Am J Ophthalmol 131:647–652PubMedCrossRef
15.
Zurück zum Zitat Rammensee HG, Friede T, Stevanovic S (1995) MHC ligands and peptide motifs: first listing. Immunogenetics 41:178–228PubMedCrossRef Rammensee HG, Friede T, Stevanovic S (1995) MHC ligands and peptide motifs: first listing. Immunogenetics 41:178–228PubMedCrossRef
16.
Zurück zum Zitat Hill CM, Liu A, Marshall KW, et al (1994) Exploration of requirements for peptide binding to HLA DRB1*0101 and DRB1*0401. J Immunol 152:2890–2898PubMed Hill CM, Liu A, Marshall KW, et al (1994) Exploration of requirements for peptide binding to HLA DRB1*0101 and DRB1*0401. J Immunol 152:2890–2898PubMed
17.
Zurück zum Zitat Shichijo S, Nakao M, Imai Y, et al (1998) A gene encoding antigenic peptides of human squamous cell carcinoma recognized by cytotoxic T lymphocytes. J Exp Med 187:277–288PubMedCrossRef Shichijo S, Nakao M, Imai Y, et al (1998) A gene encoding antigenic peptides of human squamous cell carcinoma recognized by cytotoxic T lymphocytes. J Exp Med 187:277–288PubMedCrossRef
18.
Zurück zum Zitat Kimura H, Morita M, Yabuta Y, et al (1999) Quantitative analysis of Epstein–Barr virus load by using a real-time PCR assay. J Clin Microbiol 37:132–136PubMed Kimura H, Morita M, Yabuta Y, et al (1999) Quantitative analysis of Epstein–Barr virus load by using a real-time PCR assay. J Clin Microbiol 37:132–136PubMed
19.
Zurück zum Zitat Linhares MI, de Andrade GP, Tateno S, et al (1989) Prevalence of cytomegalovirus antibodies in Brazilian and Japanese populations in the north-east of Brazil. Microbiol Immunol 33:975–980PubMed Linhares MI, de Andrade GP, Tateno S, et al (1989) Prevalence of cytomegalovirus antibodies in Brazilian and Japanese populations in the north-east of Brazil. Microbiol Immunol 33:975–980PubMed
20.
Zurück zum Zitat Topalian SL, Gonzales MI, Parkhurst M, et al (1996) Melanoma-specific CD4+ T cells recognize nonmutated HLA-DR-restricted tyrosinase epitopes. J Exp Med 183:1965–1970PubMedCrossRef Topalian SL, Gonzales MI, Parkhurst M, et al (1996) Melanoma-specific CD4+ T cells recognize nonmutated HLA-DR-restricted tyrosinase epitopes. J Exp Med 183:1965–1970PubMedCrossRef
21.
Zurück zum Zitat Wildner G, Diedrichs-Mohring M, Thurau SR (2002) Induction of arthritis and uveitis in Lewis rats by antigenic mimicry of peptides from HLA-B27 and cytokeratin. Eur J Immunol 32:299–306PubMedCrossRef Wildner G, Diedrichs-Mohring M, Thurau SR (2002) Induction of arthritis and uveitis in Lewis rats by antigenic mimicry of peptides from HLA-B27 and cytokeratin. Eur J Immunol 32:299–306PubMedCrossRef
22.
Zurück zum Zitat Singh VK, Kalra HK, Yamaki K, et al (1990) Molecular mimicry between uveitopathogenic site of S-antigen and viral peptides. J Immunol 144:1282–1287PubMed Singh VK, Kalra HK, Yamaki K, et al (1990) Molecular mimicry between uveitopathogenic site of S-antigen and viral peptides. J Immunol 144:1282–1287PubMed
23.
Zurück zum Zitat Rasmussen L (1990) Immune response to human cytomegalovirus infection. Curr Top Microbiol Immunol 154:221–254PubMed Rasmussen L (1990) Immune response to human cytomegalovirus infection. Curr Top Microbiol Immunol 154:221–254PubMed
24.
Zurück zum Zitat Chou S (1992) Molecular epidemiology of envelope glycoprotein H of human cytomegalovirus. J Infect Dis 166:604–607PubMed Chou S (1992) Molecular epidemiology of envelope glycoprotein H of human cytomegalovirus. J Infect Dis 166:604–607PubMed
Metadaten
Titel
Cross-reaction between tyrosinase peptides and cytomegalovirus antigen by T cells from patients with Vogt-Koyanagi-Harada disease
verfasst von
Sunao Sugita
Hiroshi Takase
Tatsushi Kawaguchi
Chikako Taguchi
Manabu Mochizuki
Publikationsdatum
01.06.2007
Verlag
Kluwer Academic Publishers
Erschienen in
International Ophthalmology / Ausgabe 2-3/2007
Print ISSN: 0165-5701
Elektronische ISSN: 1573-2630
DOI
https://doi.org/10.1007/s10792-006-9020-y

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