IL-18 not required for IRBP peptide-induced EAU: studies in gene-deficient mice

Hui-Rong Jiang, X. Wei, W. Niedbala, Lynne Lumsden, F. Y. Liew, John Vincent Forrester

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

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 IL-18(-/-) phenotype.

METHODS. IL-18 detection was performed by using 5-bromo-4-chloro-3-indoyl-beta -D-galactopyranoside (X-Gal) staining on frozen sections of eps 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(129/CD1, DBA1, and Balb/c), either of normal phenotype (+/+) or of deficiency (+/-, -/-) in the IL-18 gene which had been replaced by introduced genes including LacZ under the control of an IL-18 promotor.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 (va) 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)-gamma and tumor necrosis factor (TNF)-alpha 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 undetermined.

Original languageEnglish
Pages (from-to)177-182
Number of pages5
JournalInvestigative Ophthalmology & Visual Science
Volume42
Issue number1
Publication statusPublished - 2001

Keywords

  • EXPERIMENTAL AUTOIMMUNE UVEORETINITIS
  • INTERFERON-GAMMA PRODUCTION
  • IL-18-DEFICIENT MICE
  • COSTIMULATORY FACTOR
  • CYTOKINE PRODUCTION
  • DENDRITIC CELLS
  • TH2 CELLS
  • T-CELLS
  • INDUCTION
  • INTERLEUKIN-18

Cite this

Jiang, H-R., Wei, X., Niedbala, W., Lumsden, L., Liew, F. Y., & Forrester, J. V. (2001). IL-18 not required for IRBP peptide-induced EAU: studies in gene-deficient mice. Investigative Ophthalmology & Visual Science, 42(1), 177-182.

IL-18 not required for IRBP peptide-induced EAU: studies in gene-deficient mice. / Jiang, Hui-Rong; Wei, X.; Niedbala, W.; Lumsden, Lynne; Liew, F. Y.; Forrester, John Vincent.

In: Investigative Ophthalmology & Visual Science, Vol. 42, No. 1, 2001, p. 177-182.

Research output: Contribution to journalArticle

Jiang, H-R, Wei, X, Niedbala, W, Lumsden, L, Liew, FY & Forrester, JV 2001, 'IL-18 not required for IRBP peptide-induced EAU: studies in gene-deficient mice', Investigative Ophthalmology & Visual Science, vol. 42, no. 1, pp. 177-182.
Jiang H-R, Wei X, Niedbala W, Lumsden L, Liew FY, Forrester JV. IL-18 not required for IRBP peptide-induced EAU: studies in gene-deficient mice. Investigative Ophthalmology & Visual Science. 2001;42(1):177-182.
Jiang, Hui-Rong ; Wei, X. ; Niedbala, W. ; Lumsden, Lynne ; Liew, F. Y. ; Forrester, John Vincent. / IL-18 not required for IRBP peptide-induced EAU: studies in gene-deficient mice. In: Investigative Ophthalmology & Visual Science. 2001 ; Vol. 42, No. 1. pp. 177-182.
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abstract = "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 IL-18(-/-) phenotype.METHODS. IL-18 detection was performed by using 5-bromo-4-chloro-3-indoyl-beta -D-galactopyranoside (X-Gal) staining on frozen sections of eps 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 (va) 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)-gamma and tumor necrosis factor (TNF)-alpha 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 undetermined.",
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T1 - IL-18 not required for IRBP peptide-induced EAU: studies in gene-deficient mice

AU - Jiang, Hui-Rong

AU - Wei, X.

AU - Niedbala, W.

AU - Lumsden, Lynne

AU - Liew, F. Y.

AU - Forrester, John Vincent

PY - 2001

Y1 - 2001

N2 - 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 IL-18(-/-) phenotype.METHODS. IL-18 detection was performed by using 5-bromo-4-chloro-3-indoyl-beta -D-galactopyranoside (X-Gal) staining on frozen sections of eps 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 (va) 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)-gamma and tumor necrosis factor (TNF)-alpha 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 undetermined.

AB - 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 IL-18(-/-) phenotype.METHODS. IL-18 detection was performed by using 5-bromo-4-chloro-3-indoyl-beta -D-galactopyranoside (X-Gal) staining on frozen sections of eps 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 (va) 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)-gamma and tumor necrosis factor (TNF)-alpha 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 undetermined.

KW - EXPERIMENTAL AUTOIMMUNE UVEORETINITIS

KW - INTERFERON-GAMMA PRODUCTION

KW - IL-18-DEFICIENT MICE

KW - COSTIMULATORY FACTOR

KW - CYTOKINE PRODUCTION

KW - DENDRITIC CELLS

KW - TH2 CELLS

KW - T-CELLS

KW - INDUCTION

KW - INTERLEUKIN-18

M3 - Article

VL - 42

SP - 177

EP - 182

JO - Investigative Ophthalmology & Visual Science

JF - Investigative Ophthalmology & Visual Science

SN - 0146-0404

IS - 1

ER -