Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/ijms22041553
Keywords
SWI3-related gene (SRG3); atopic dermatitis; Th2 cells; Treg cells; NC; Nga; WT
Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [NRF-2018R1D1A1A02086057, NRF-2018R1D1A1B07049495, NRF-2016R1D1A1A09919293, NRF-2019R1A2C1 009926]
- National Research Foundation of Korea [4199990314450] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The overexpression of SRG3 has been shown to accelerate the development of AD in mice, leading to increased clinical severity and immune cell infiltration in skin lesions. This enhanced pathogenesis is linked to the expansion of IL-4-producing cells and suppression of Treg cells, suggesting that modulation of SRG3 function may be a potential therapeutic option for controlling AD.
The SWItch (SWI)3-related gene (SRG3) product, a SWI/Sucrose Non-Fermenting (SNF) chromatin remodeling subunit, plays a critical role in regulating immune responses. We have previously shown that ubiquitous SRG3 overexpression attenuates the progression of Th1/Th17-mediated experimental autoimmune encephalomyelitis. However, it is unclear whether SRG3 overexpression can affect the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD), a Th2-type immune disorder. Thus, to elucidate the effects of SRG3 overexpression in AD development, we bred NC/Nga (NC) mice with transgenic mice where SRG3 expression is driven by the beta-actin promoter (SRG3(beta-actin) mice). We found that SRG3(beta-actin) NC mice exhibit increased AD development (e.g., a higher clinical score, immunoglobulin E (IgE) hyperproduction, and an increased number of infiltrated mast cells and basophils in skin lesions) compared with wild-type NC mice. Moreover, the severity of AD pathogenesis in SRG3(beta-actin) NC mice correlated with expansion of interleukin 4 (IL4)-producing basophils and mast cells, and M2 macrophages. Furthermore, this accelerated AD development is strongly associated with Treg cell suppression. Collectively, our results have identified that modulation of SRG3 function can be applied as one of the options to control AD pathogenesis.
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