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

• DOI: 10.1007/s10792-006-9020-y
• Publication Date: 2007-01-25T08:48:26Z
• Authors: Sunao Sugita; Hiroshi Takase; Tatsushi Kawaguchi; Chikako Taguchi; Manabu Mochizuki
• Keywords: Herpesvirus 3, Human; Herpesvirus 4, Human; Monophenol Monooxygenase; Reverse Transcriptase Polymerase Chain Reaction; T-Lymphocytes; Complement Fixation Tests; Molecular Mimicry; Antigen-Presenting Cells; Cytomegalovirus; Genome, Viral; Cross Reactions; Lymphocyte Activation; Peptide Fragments; 3. Good health; 03 medical and health sciences; 0302 clinical medicine; Viral Envelope Proteins; Seroepidemiologic Studies; DNA, Viral; Cytokines; Humans; Simplexvirus; Uveomeningoencephalitic Syndrome

To determine whether T lymphocytes of patients with Vogt-Koyanagi-Harada (VKH) disease cross-react with peptides of melanocytes and with exogenous antigens.Cross-reactivity with melanocyte peptides, tyrosinase (tyrosinase(450-462): SYLQDSDPDSFQD) and the mimic virus peptide, i.e., cytomegalovirus envelope glycoprotein H (CMV-egH(290-302): 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).Some of the T cells established from VKH recognized melanocyte peptides including the tyrosinase peptide as well as the CMV-egH(290-302) 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-egH(290-302) but also to tyrosinase(450-462). The seroprevalence of CMV was significantly higher in VKH patients. In addition, all tested samples of VKH patients were negative for CMV-DNA.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.