A novel inflammatory eye disease induced by lymphocytes from knockout mice sensitized against the deleted ocular antigen

M. P. Gelderman, P. Charukamnoetkanok, J. P. Brady, L. Hung, J. S. Zigler, E. F. Wawrousek, B. P. Vistica, E. Fortin, C. C. Chan, Igal Gery

Research output: Contribution to journalArticlepeer-review

Abstract

Lens-associated uveitis (LAU), a severe inflammatory eye disease, is thought to be mediated by autoimmunity against lens crystallins. Previously described animal models for this disease are antibody-mediated, since no cellular response to self crystallins could be induced in experimental animals. Here, we describe a new model for LAU, in which lymphocytes from knockout mice deficient in αB-crystallin are sensitized against the deleted protein and induce severe ocular inflammation when adoptively transferred into wild type recipients. Similar to LAU, the experimental disease developed only following rupture of the lens capsule, produced in this study by capsulotomy; no disease was detected in recipient eyes with no capsulotomy, or in those treated with cautery, or in eyes affected by systemic treatment with sodium iodate, lipopolysaccharide or X-irradiation. The ocular changes in affected eyes included heavy cellular infiltration and proteinaceous exudate in both the anterior and posterior segments of the eye, that reached their peak on day 4 following cell transfer and subsided quite rapidly thereafter.

Original languageEnglish (US)
Pages (from-to)177-181
Number of pages5
JournalClinical and Experimental Immunology
Volume133
Issue number2
DOIs
StatePublished - Aug 1 2003

Keywords

  • Autoimmunity
  • Inflammation
  • Knockout mice
  • Lens-associated uveitis
  • α-crystallin

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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