Lymphotoxin β receptor-lg fusion protein treatment blocks actively induced, but not adoptively transferred, uveitis in Lewis rats

Hui Shao, Yangxin Fu, Lei Song, Sheler Sun, Herry J. Kaplan, Deming Sun

Research output: Contribution to journalArticle

26 Scopus citations


Previous studies have shown that treatment of rodents with a lymphotoxin (LT)-β receptor-Ig fusion protein (LTβR-Ig), which binds to both LT and LIGHT, prevents the development of autoimmune diseases, but the mechanism involved is unclear. To explore the potential role of LT or LIGHT in the pathogenesis of autoimmune uveitis, uveitis was induced in Lewis rats either by immunization with an uveitogenic peptide, R16, derived from the interphotoreceptor retinoid-binding protein, or by adoptive transfer of R16-specific T cells. Interestingly, LTβR-Ig treatment completely prevented actively induced uveitis, but not the adoptively transferred disease. We also show that LTβR-Ig-treated R16-injected rats had a significantly decreased T cell response to R16 and that herpesvirus entry mediator (HVEM)-Ig, a fusion protein that blocks LIGHT, also inhibited disease development. Our results suggest that LT or LIGHT plays a critical role in the induction, rather than the effector, phase of the disease.

Original languageEnglish (US)
Pages (from-to)1736-1743
Number of pages8
JournalEuropean Journal of Immunology
Issue number6
StatePublished - Jun 1 2003



  • Autoimmunity
  • Costimulation
  • Interphotoreceptor retinoid-binding protein
  • Lymphotoxin β receptor-lg fusion protein
  • Uveitis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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