Defective natural killer cell activity in a mouse model of eczema herpeticum
- Authors
- Kawakami, Yuko; Ando, Tomoaki; Lee, Jong-Rok; Kim, Gisen; Kawakami, Yu; Nakasaki, Tae; Nakasaki, Manando; Matsumoto, Kenji; Choi, Youn Soo; Kawakami, Toshiaki
- Issue Date
- Mar-2017
- Publisher
- MOSBY-ELSEVIER
- Keywords
- Atopic dermatitis; eczema herpeticum; herpes simplex virus; animal model; natural killer cell
- Citation
- JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, v.139, no.3, pp.997 - +
- Journal Title
- JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
- Volume
- 139
- Number
- 3
- Start Page
- 997
- End Page
- +
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/6342
- DOI
- 10.1016/j.jaci.2016.06.034
- ISSN
- 0091-6749
- Abstract
- Background: Patients with atopic dermatitis (AD) are susceptible to several viruses, including herpes simplex virus (HSV). Some patients experience 1 or more episodes of a severe skin infection caused by HSV termed eczema herpeticum (EH). There are numerous mouse models of AD, but no established model exists for EH. Objective: We sought to establish and characterize a mouse model of EH. Methods: We infected AD-like skin lesions with HSV1 to induce severe skin lesions in a dermatitis-prone mouse strain of NC/Nga. Gene expression was investigated by using a microarray and quantitative PCR; antibody titers were measured by means of ELISA; and natural killer (NK) cell, cytotoxic T-cell, regulatory T-cell, and follicular helper T-cell populations were evaluated by using flow cytometry. The role of NK cells in HSV1-induced development of severe skin lesions was examined by means of depletion and adoptive transfer. Results: InoculationofHSV1inducedsevereerosiveskinlesionsin eczematousmice, which had an impaired skinbarrier, butmilder lesionsinsmallnumbersofnormalmice. Eczematousmiceexhibited lowerNKcellactivitybutsimilarcytotoxicT-cellactivityand humoralimmuneresponsescomparedwithnormalmice. Theroleof NKcellsincontrollingHSV1-inducedskinlesionswasdemonstrated byexperimentsdepletingortransferringNKcells. Conclusion: A murine model of EH with an impaired skin barrier was established in this study. We demonstrated a critical role of defective NK activities in the development of HSV1induced severe skin lesions in eczematous mice.
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