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김서형(피부과학교실) Allergy
등록일 : 2018-04-30 오전 10:29:00       조회 : 258
첨   부 :
제1저자 신정우(피부과학교실) 김서형(피부과학교실, BK21)
교신저자 이광훈(피부과학교실)

Allergy. 2018 Apr 21. doi: 10.1111/all.13465. [Epub ahead of print]
Allergen-specific immunotherapy induces regulatory T cells in an atopic dermatitis mouse model.
Shin JU1, Kim SH1,2, Noh JY1, Kim JH1,2, Hye Ran K1, Jeong KY3, Park KH3, Lee J1, Chu H1, Lee JH3, Yong TS4, Park JW3, Lee KH1,2.

Author information
1Department of Dermatology & Cutaneous Biology Research Institute.2Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.3Department of Internal Medicine, Institute of Allergy, Yonsei University College of Medicine, Seoul, Korea.4Department of Environmental Medical Biology, Institute of Tropical Medicine, Arthropds of Medical Importance Resource Bank, Yonsei University College of Medicine, Seoul, Korea.

Abstract
BACKGROUND:
Several studies have demonstrated that allergen-specific immunotherapy (SIT) can be an effective treatment for atopic dermatitis (AD). However, there is no relevant mouse model to investigate the mechanism and validate the novel modality of SIT in AD.
METHODS:
NC/Nga mice with induced AD-like skin lesions received a subcutaneous injection of SIT (an extract of the house dust mite Dermatophagoides farinae [DfE]) or placebo for 5 weeks). Clinical and histological improvements of AD-like skin lesions were examined. The responses of local and systemic regulatory T (Treg) cells, natural killer (NK) cells, B cells, serum immunoglobulin, and T-cell cytokine response to DfE were evaluated to determine the underlying mechanism of the observed results.
RESULTS:
SIT significantly improved AD-like skin lesions. Histologically, SIT decreased epidermal thickness and reduced inflammatory cell infiltration, especially that of eosinophils. Concomitantly, SIT suppressed Th2 responses and induced local infiltration of Treg cells into the skin. Also SIT induced the immunoglobulin G4 and attenuated allergen-specific immunoglobulin E. Furthermore, SIT induced local and systemic IL-10-producing Treg cells and regulatory NK cells.
CONCLUSION:
We established a SIT model on AD mice and showed that our model correlates well with previous reports about SIT-treated patients. Also we revealed NK cells as another possible resource of IL-10 in SIT. Based on our results, we suggest our SIT model as a useful tool to investigate mechanism of action of SIT and to validate the efficacy of new SIT modalities for the treatment of AD. This article is protected by copyright. All rights reserved.
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