Impacts of GFP-FoxP3(+) regulatory T cells on lupus hallmarks differ by genetic background and type of GFP knock-in
- Authors
- Chang, Soog-Hee; Kim, Tae-Joo; Kim, Yongbaek; Han, Seung Seok; Lee, Sun-Kyung; Sim, Ji Hyun; Kim, Young-Joo; Lee, Se Jeong; Rhyu, Im Joo; Nam, Ki-Hoan; Mohan, Chandra; Kim, Hang-Rae
- Issue Date
- 18-8월-2019
- Publisher
- TAYLOR & FRANCIS LTD
- Keywords
- anti-nuclear antibodies; green fluorescence protein; lupus; Regulatory T cells; Sle1 gene locus
- Citation
- AUTOIMMUNITY, v.52, no.5-6, pp.199 - 207
- Indexed
- SCIE
SCOPUS
- Journal Title
- AUTOIMMUNITY
- Volume
- 52
- Number
- 5-6
- Start Page
- 199
- End Page
- 207
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/63505
- DOI
- 10.1080/08916934.2019.1657098
- ISSN
- 0891-6934
- Abstract
- FoxP3 reporter mice expressing green fluorescence protein (GFP) have been used as a very convenient tool to investigate the impact of regulatory T (Treg) cells on pathogenesis in autoimmune diseases. Here, we found that GFP-FoxP3(+) knock-in (KI) mice showed alterations in the production of anti-nuclear autoantibodies (ANAs) and nephritis with different extent, depending on the presence or absence of lupus susceptibility gene locus 1 (Sle1) and KI method: contrasting with B6.Sle1.fGFP-FoxP3 mice, expressing GFP via N-terminal insertion, B6.Sle1.iGFP-FoxP3, expressing GFP via bicistronic internal ribosome entry site-driven promotion, exhibited significantly lower penetrance of serum ANA, comparing to control B6.Sle1 mice. Moreover, B6.Sle1.GFP-FoxP3(+) mice reduced the Sle1-induced splenomegaly and B-cell expansion independently of the KI method employed, mainly by reducing the numbers of transitional 1 (T1) B cells and CD21(-)CD23(-) B cells, including plasmablasts and plasma cells. The absolute numbers of both splenic CD4(+) T cells and Treg cells from B6.Sle1.GFP-FoxP3 KI mice were significantly reduced but their proportion was not changed, compared to B6.Sle1 mice. Although the glomerular basement membranes were thickened in both B6.Sle1 and B6.Sle1.iGFP-FoxP3 mice, they were thinner in B6.Sle1.fGFP-FoxP3 mice. The latter mice expressed more nephrophilic autoantibodies and deposited more complement component 3 in glomeruli compared to B6.iGFP-FoxP3 mice. FoxP3(+) Treg cells may modulate B-cell tolerance in lupus-prone B6.Sle1 mice, presumably by modulating pathogenic, nephrophilic autoantibody production and nephritis.
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