Ubiquitous Overexpression of Chromatin Remodeling Factor SRG3 Exacerbates Atopic Dermatitis in NC/Nga Mice by Enhancing Th2 Immune Responses
| Autor: | Jungmin Jeon, Rho Hyun Seong, Yun Hoo Park, Luc Van Kaer, Tae-Cheol Kim, Sung Won Lee, Seokmann Hong, Sung Ho Jeon, Hyun Jung Park |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
SWI3-related gene (SRG3)
Biopsy Chromatin Remodeling Factor Gene Expression Mice Transgenic Biology Immunoglobulin E Severity of Illness Index Catalysis Chromatin remodeling Article Dermatitis Atopic Inorganic Chemistry Pathogenesis lcsh:Chemistry Mice Immune system medicine Animals Physical and Theoretical Chemistry Molecular Biology lcsh:QH301-705.5 Spectroscopy Interleukin 4 Immunity Cellular atopic dermatitis WT Macrophages Organic Chemistry Experimental autoimmune encephalomyelitis General Medicine Dendritic Cells medicine.disease Chromatin Assembly and Disassembly Actins Computer Science Applications NC/Nga Disease Models Animal Th2 cells lcsh:Biology (General) lcsh:QD1-999 Immunology biology.protein Immune disorder Disease Susceptibility Treg cells Transcription Factors |
| Zdroj: | International Journal of Molecular Sciences, Vol 22, Iss 1553, p 1553 (2021) International Journal of Molecular Sciences Volume 22 Issue 4 |
| ISSN: | 1661-6596 1422-0067 |
| Popis: | 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 β-actin promoter (SRG3β-actin mice). We found that SRG3β-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 SRG3β-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. |
| Databáze: | OpenAIRE |
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