title: Role of T-cell receptor V beta 8.3 peptide vaccine in the prevention of experimental autoimmune uveoretinitis.
abstract: BACKGROUND
  T-cell receptor (TCR) plays an important role in the development of autoimmune diseases. Recently, it was reported that immunization of animals with TCR peptide derived from the pathogenic cells could prevent autoimmune diseases. The aim of this study was to investigate whether vaccination with a synthetic peptide from the hypervariable region of TCR V(beta) 8.3, an experimental autoimmune uveoretinitis (EAU)-associated gene, was able to prevent the disease.
  
  
  METHODS
  EAU was induced in Lewis rats by immunization with IRBP R16 peptide emulsified in complete Freund's adjuvant (CFA). The clinical and histological appearances were scored. Delayed type hypersensitivity (DTH) and lymphocyte proliferation were detected. Cytokine levels of aqueous humour, supernatants of cells from spleen and draining lymph nodes were measured by enzyme linked immunosorbent assay (ELISA). Gene expression of TCR V(beta) 8.3 on CD(4)(+) T cells was examined by real time quantitative polymerase chain reaction (PCR).
  
  
  RESULTS
  After vaccination, the intraocular inflammation was significantly mitigated, antigen specific DTH and lymphocyte proliferation responses were suppressed, interleukin (IL)-2 in aqueous humour, interferon (IFN)-gamma and IL-2 produced by the spleen and draining lymph node cells were significantly decreased, whereas the production of IL-4 and IL-10 were increased. The response of draining lymph node cells to TCR V(beta) 8.3 peptide was enhanced after vaccination. Inoculation with CFA alone did not affect the severity of EAU and the above parameters. The suppression of EAU was much stronger in the group of four fold inoculations than the group of two fold inoculations. The expression of TCR V(beta) 8.3 gene was significantly reduced in the group of fourfold inoculations.
  
  
  CONCLUSIONS
  Vaccination with the synthetic TCR V(beta) 8.3 peptide could remarkably inhibit the development of EAU.
authors.affiliation: Zhongshan Ophthalmic Centre, Sun Yat-sen University, Guangzhou 510060, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Zhang
authors.forename: Pei-zeng
authors.initials: PZ
authors.lastname: Yang
authors.forename: Chang-you
authors.initials: CY
authors.lastname: Wu
authors.forename: Hao-li
authors.initials: HL
authors.lastname: Jin
authors.forename: Bing
authors.initials: B
authors.lastname: Li
authors.forename: Xiang-kun
authors.initials: XK
authors.lastname: Huang
authors.forename: Hong-yan
authors.initials: HY
authors.lastname: Zhou
authors.forename: Yang
authors.initials: Y
authors.lastname: Gao
authors.forename: Lian-xiang
authors.initials: LX
authors.lastname: Zhu
authors.forename: Aize
authors.initials: A
authors.lastname: Kijlstra
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000517:prevention & control*; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D019674:Genes, T-Cell Receptor beta; D051381:Rats; D011917:Rats, Inbred Lew; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*; D012173:Retinitis / Q000517:prevention & control*; D012177:Retinol-Binding Proteins / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014605:Uveitis / Q000517:prevention & control*; D014611:Vaccination; D000099214:Retinol-Binding Proteins, Interstitial
chemical_list: D016207:Cytokines; D016693:Receptors, Antigen, T-Cell, alpha-beta; D012177:Retinol-Binding Proteins; C487847:Rbp3 protein, rat; D000099214:Retinol-Binding Proteins, Interstitial