Mice deficient in inducible nitric oxide synthase are susceptible to experimental autoimmune uveoretinitis.

Journal Article (Journal Article)

PURPOSE: Nitric oxide (NO) is an important mediator of inflammatory tissue damage. The present study addresses the question whether inducible nitric oxide synthase (iNOS), and consequently the ability to upregulate NO, is required to effect the pathogenesis of experimental autoimmune uveoretinitis (EAU) in mice. METHODS: Mice with a homologous disruption of the iNOS gene (iNOS KO) were evaluated for their ability to develop EAU and associated cellular responses after immunization with the interphotoreceptor retinoid-binding protein. EAU was determined by histopathology 21 days after uveitogenic immunization, and antigen-specific cellular responses were assessed by delayed type hypersensitivity and lymphocyte proliferation. RESULTS: iNOS knockout (iNOS KO) mice developed EAU with scores similar to wild-type mice and exhibited good cellular responses to the immunizing antigen. CONCLUSIONS: A functional iNOS gene is not necessary for EAU pathogenesis. Therefore, upregulation of NO is not required to mediate autoimmune tissue damage in the eye.

Full Text

Duke Authors

Cited Authors

  • Silver, PB; Tarrant, TK; Chan, CC; Wiggert, B; Caspi, RR

Published Date

  • May 1999

Published In

Volume / Issue

  • 40 / 6

Start / End Page

  • 1280 - 1284

PubMed ID

  • 10235566

International Standard Serial Number (ISSN)

  • 0146-0404


  • eng

Conference Location

  • United States