Innate Type 2 Response to Aspergillus fumigatus in a Murine Model of Atopic Dermatitis-like Skin Inflammation

Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease mediated by T helper type 2 (Th2) cells in acute phase. Group 2 innate lymphoid cells (ILCs) play a role in the initiation of the Th2 response. Although mold exposure is associated with the development of AD, studies on the...

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Veröffentlicht in:Journal of Korean medical science 2021, 36(40), , pp.1-12
Hauptverfasser: Park, Arum, Lee, Eun, Park, Hyojung, Park, Mee-Na, Lee, Jiho, Song, Kun Baek, Yoon, Jisun, Jung, Sungsu, Suh, Nayoung, Yoon, Jin, Yu, Jinho
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Sprache:eng
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Zusammenfassung:Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease mediated by T helper type 2 (Th2) cells in acute phase. Group 2 innate lymphoid cells (ILCs) play a role in the initiation of the Th2 response. Although mold exposure is associated with the development of AD, studies on the underlying mechanisms are lacking. This study investigated whether group 2 ILCs are involved in inflammation in AD-like skin induced by ( ). We investigated changes of group 2 ILCs population in -induced AD-like skin lesions. To induce AD-like skin lesions, extracts were applied to the dorsal skin of BALB/c and mice five times per week, with repeat exposures at 2-week intervals. The clinical parameters were higher in the -treated group than in the control group. Histologic findings revealed epiderrmal and dermal thickening as well as eosinophil and mast cell infiltration into the skin of -treated mice. Populations of group 2 ILCs in the skin were also significantly higher in the -treated group. In addition, interleukin-33 mRNA expression was significantly higher in the skin lesions of the -treated mice. In the mice lacking mature lymphocytes, AD-like skin lesions were still induced by and ILCs depletion using an anti-CD90.2 mAb lowered the -induced inflammatory response. Group 2 ILCs may play a role in a murine model of -induced AD-like skin lesions.
ISSN:1011-8934
1598-6357
DOI:10.3346/jkms.2021.36.e261