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Article |
B
-/- mice
1 Department of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan
2 Department of Dermatology,, Kyoto Prefectural University of Medicine, Kyoto, Japan
3 Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka, Japan
4 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan
* To whom correspondence should be addressed. E-mail: mueta{at}ophth.kpu-m.ac.jp.
| Abstract |
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Purpose: I
B
-/- mice were reported to be affected by allergic dermatitis. To analyze the pathophysiological role of I
B
and to address the functional relevance of Th2-mediated immune responses in the development of ocular surface inflammation and dermatitis by I
B
-/- mice.
Methods: We established Balb/c background I
B
-/- mice without individual differences, created I
B
/Stat6 double-knock-out (WKO) mice unable to produce Th2 cytokine, and performed microscopic-, histological-, and immunochemical studies. In I
B
-/- mice we examined the serum IgE levels by ELISA and used quantitative PCR to study the gene expression of IFN-
, IL4, IL10, TNF
, IL6, IL17
, and CCL11 in eyelid tissue.
Results: I
B
-/- 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-positive cells; in the conjunctiva we mainly detected CD4- and CD45R/B220-positive cells. In eyelid and perioral skin tissue the expression of IL-17
and of Th1 and Th2 cytokines, but not of CCL11, was augmented. I
B
-/- and I
B
-/+ mice did not differ significantly in their serum total IgE levels before- and 0-4- and 5-9 weeks after disease onset. I
B
/Stat6 WKO mice elicited the same or a little more severe inflammation than that of I
B
-/- mice.
Conclusion: IgE and Stat6 are not responsible for the immune-pathological response leading to the development of ocular surface and perioral skin inflammation in I
B
-/- mice. I
B
-/- mice might be a suitable model for Stevens-Johnson syndrome (SJS), but not atopic dermatitis.
Key Words:
I
B
-/- mice, ocular surface inflammation, Stevens-Johnson syndrome, dermatitis, Stat6
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