SLAT/Def6 knock-out (KO) mice exhibit profoundly reduced capacity to develop experimental autoimmune uveitis (EAU)

Wednesday, October 26, 2011 — Poster Session IV
2:00 p.m. – 4:00 p.m.	Natcher Conference Center	NEI	IMMUNO/INFLAM-30

Authors

• B Vistica
• G Shi
• L Nugent
• A Altman
• I Gery

Abstract

SWAP 70-like adapter of T cells (SLAT; aka Def6) is a recently discovered protein that plays a role in CD4+ T cell activation and autoimmunity. We investigated the role of SLAT/Def6 in the development of EAU, an animal model for several uveitic conditions in humans. KO mice and C57Bl/6 controls were immunized, with interphotoreceptor-retinoid binding protein (IRBP), emulsified with CFA, along with pertussis toxin. The development of ocular inflammation was determined by fundoscopy on day 12 and by histological examination on day 14, post-immunization. Draining lymph node cells were cultured with IRBP to measure proliferation and release of IFN-g and IL-17. Serum antibody to IRBP was measured by ELISA. qPCR compared the transcript levels of IFN-g and IL-17 in inflamed eyes. KO mice had reduced EAU, and exhibited impaired proliferation and production of IFN-g and IL-17. In contrast, antibody to IRBP was essentially the same in KO mice and controls. qPCR of inflamed eyes detected similar levels of IFN-g transcript in control and KO mice, whereas the IL-17 transcript levels in KO eyes were strikingly lower. These data provide new evidence to show that SLAT/Def6 is a regulator of inflammatory response.

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