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Hui-Rong Jiang, Xiao-qing Wei, Wanda Niedbala, Lynne Lumsden, Foo Yew Liew, John V. Forrester; IL-18 Not Required for IRBP Peptide–Induced EAU: Studies in Gene-Deficient Mice. Invest. Ophthalmol. Vis. Sci. 2001;42(1):177-182.
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purpose. Interleukin (IL)-18 has been described as a proinflammatory cytokine in
rheumatoid arthritis and bacterial infectious diseases. The present
study was designed to determine the role of IL-18 in a model of ocular
experimental autoimmune uveitis (EAU). The initial studies were
conducted to detect the expression of IL-18 in normal mouse eye tissue,
and the later studies investigated induction of EAU in mice with an
methods. IL-18 detection was performed by using
staining on frozen sections of eyes from mice (129/CD1, DBA1, and
Balb/c), either of normal phenotype (+/+) or of deficiency (±, −/−)
in the IL-18 gene which had been replaced by
introduced genes including LacZ under the control of an
IL-18 promotor. Severity of EAU was assessed in DBA1 and 129/CD1
wild-type (WT) or IL-18 knockout (KO) mice after immunization with the
uveitogenic antigen: interphotoreceptor retinal binding protein (IRBP)
peptide 161-180. Lymphocyte proliferation and cytokine production were
also measured in WT and IL-18 KO DBA1 mice 15 days after immunization.
results. IL-18 is constitutively expressed in the epithelial cells in iris,
ciliary body, and retina. EAU-resistant mice (129/CD1) with an
IL-18−/− phenotype remained resistant after immunization
with IRBP peptide (P161-180). However, EAU-susceptible mice (DBA1)
exhibited disease with similar histologic characteristics, despite a
generalized reduction of interferon (IFN)-γ and tumor necrosis factor
(TNF)-α on an IL-18−/− phenotype. DBA1
IL-18−/− also demonstrated reduced IL-10 production.
conclusions. The IL-18 gene is not necessary for the initiation or
pathogenesis of EAU induced by IRBP peptide 161-180. IL-18 is expressed in the epithelial cells in iris,
ciliary body, and retina in the eyes, but its role in the eye remains
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