title: IFN-β inhibits the increased expression of IL-9 during experimental autoimmune uveoretinitis.
abstract: OBJECTIVE
  It has been shown that IL-9 plays a proinflammatory role in the pathogenesis of certain autoimmune diseases. This study was designed to investigate the possible role of IL-9 in the development of experimental autoimmune uveoretinitis (EAU) and the effect of IFN-β on its expression.
  
  
  METHODS
  EAU was induced in B10RIII mice by immunization with interphotoreceptor retinoid-binding protein peptide 161-180 (IRBP(161-180)). IFN-β was administered subcutaneously to IRBP(161-180) immunized mice every other day from day one before immunization to the end of the study. Splenocytes and draining lymph node (DLN) cells from EAU mice or control mice or EAU mice treated with IFN-β or PBS were stimulated with anti-CD3/CD28 or IRBP(161-180) for 3 days. Naïve T cells cultured under Th1 or Th17 polarizing conditions were incubated in the presence or absence of IFN-β for 4 days. Effector/memory T cells were activated by anti-CD3/CD28 in the presence or absence of IFN-β for 3 days. IFN-β-treated monocytes were cocultured with naïve T cells or effector/memory T cells for 3 days. Culture supernatants were collected and IL-9 was detected by ELISA.
  
  
  RESULTS
  IL-9 expression in splenocytes and DLN cells was increased in EAU mice during the inflammatory phase and returned back to lower levels during the recovery phase. IFN-β in vivo treatment significantly inhibited EAU activity in association with a down-regulated expression of IL-9. In vitro polarized Th1 and Th17 cells both secreted IL-9 and the addition of IFN-β suppressed production of IL-9 by both Th subsets. Beside its effect on polarized Th cells, IFN-β also suppressed the secretion of IL-9 by effector/memory T cells. However, IFN-β-treated monocytes had no effect on the production of IL-9 when cocultured with naïve or effector/memory T cells.
  
  
  CONCLUSIONS
  IL-9 expression is increased during EAU which could be suppressed by IFN-β.
authors.affiliation: Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, PR China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Yang
authors.forename: Liping
authors.initials: L
authors.lastname: Du
authors.forename: Min
authors.initials: M
authors.lastname: Sun
authors.forename: Aize
authors.initials: A
authors.lastname: Kijlstra
authors.forename: Peizeng
authors.initials: P
authors.lastname: Yang
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism*; D004195:Disease Models, Animal; D005136:Eye Proteins / Q000009:adverse effects / Q000276:immunology; D007156:Immunologic Memory; D016899:Interferon-beta / Q000008:administration & dosage / Q000494:pharmacology*; D016906:Interleukin-9 / Q000378:metabolism*; D051379:Mice; D009000:Monocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D012173:Retinitis / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism*; D012177:Retinol-Binding Proteins / Q000009:adverse effects / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology / Q000378:metabolism; D000099214:Retinol-Binding Proteins, Interstitial
chemical_list: D005136:Eye Proteins; D016899:Interferon-beta; D016906:Interleukin-9; D012177:Retinol-Binding Proteins; D000099214:Retinol-Binding Proteins, Interstitial