IOVS Molecular Human Reproduction
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Originally published In Press as doi:10.1167/iovs.08-1691 on April 25, 2008
 (Investigative Ophthalmology and Visual Science. 2008;49:3387-3394.)
© 2008 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.08-1691
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Stat6-Independent Tissue Inflammation Occurs Selectively on the Ocular Surface and Perioral Skin of I{kappa}B{zeta}–/– Mice

Mayumi Ueta,1 Junji Hamuro,1 Eiichiro Ueda,2 Norito Katoh,2 Masahiro Yamamoto,3 Kiyoshi Takeda,3 Shizuo Akira,4 and Shigeru Kinoshita1

1From the Departments of Ophthalmology and 2Dermatology, Kyoto Prefectural University of Medicine, Kyoto, Japan; the 3Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka, Japan; and the 4Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.

PURPOSE. I{kappa}B{zeta}–/– mice have been reported to be affected by allergic dermatitis. This study was conducted to analyze the pathophysiological role of I{kappa}B{zeta} and to address the functional relevance of Th2-mediated immune responses in the development of ocular surface inflammation and dermatitis by I{kappa}B{zeta}–/– mice.

METHODS. BALB/c background I{kappa}B{zeta}–/– mice were established without individual differences; I{kappa}B{zeta}/Stat6 double-knockout (WKO) mice unable to produce Th2 cytokine were created; and microscopic-, histologic-, and immunochemical studies were performed. In I{kappa}B{zeta}–/– mice the serum IgE levels were examined by ELISA, and quantitative PCR was used to study the gene expression of IFN-{gamma}, IL4, IL10, TNF{alpha}, IL6, IL17{alpha}, and CCL11 in eyelid tissue.

RESULTS. I{kappa}B{zeta}–/– mice exhibited a severe inflammatory phenotype on the ocular surface and perioral skin. The inflammatory infiltrates in the perioral skin consisted primarily of CD4+ and CD8+ cells; CD4+ and CD45R/B220+ cells were mainly detected in the conjunctiva. In eyelid and perioral skin tissue, the expression of IL-17{alpha} and of Th1 and Th2 cytokines, but not of CCL11, was augmented. I{kappa}B{zeta}–/– and I{kappa}B{zeta}+/– mice did not differ significantly in their serum total IgE levels before, 0 to 4 weeks, and 5 to 9 weeks after disease onset. I{kappa}B{zeta}/Stat6 WKO mice showed the same or slightly more severe inflammation than did I{kappa}B{zeta}–/– mice.

CONCLUSIONS. IgE and Stat6 are not responsible for the immune pathologic response leading to the development of ocular surface and perioral skin inflammation in I{kappa}B{zeta}–/– mice. I{kappa}B{zeta}–/– mice may be a suitable model for Stevens-Johnson syndrome, but not for atopic dermatitis.






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