Inhibition of IL-17 ameliorates systemic lupus erythematosus in Roquin(san/san) mice through regulating the balance of TFH cells, GC B cells, Treg and Bregopen access
- Authors
- Lee, Seon-yeong; Lee, Seung Hoon; Seo, Hyeon-Beom; Ryu, Jun-Geol; Jung, KyungAh; Choi, Jeong Won; Jhun, JooYeon; Park, Jin-Sil; Kwon, Ji Ye; Kwok, Seung-Ki; Youn, Jeehee; Park, Sung-Hwan; Cho, Mi-La
- Issue Date
- Dec-2019
- Publisher
- Nature Publishing Group
- Citation
- Scientific Reports, v.9, no.1, pp.1 - 8
- Indexed
- SCIE
SCOPUS
- Journal Title
- Scientific Reports
- Volume
- 9
- Number
- 1
- Start Page
- 1
- End Page
- 8
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/146641
- DOI
- 10.1038/s41598-019-41534-1
- ISSN
- 2045-2322
- Abstract
- Systemic lupus erythematosus (SLE) is mediated by a chronic and dysregulated inflammatory response. Interleukin (IL)-17, a proinflammatory cytokine, and T helper (Th)17 cells are associated with chronic autoimmune diseases. We hypothesized that inhibition of IL-17 would decrease the numbers of T cell subsets that function as B-cell helpers, as well as B-cell differentiation into plasma cells and autoantibody expression. The IL-17 level was increased markedly in Roquin(san/san) mice. Loss of IL-17 in Roquin(san/san) mice improved nephritis by downregulating immunoglobulin (Ig)G, IgG1, and IgG2a production. Formation of germinal centers (GCs), and follicular B- and T-cell differentiation was reduced, whereas the number of regulatory T (Treg) cells and immature B cells was increased, by IL-17 deficiency in Roquin(san/san) mice. These results suggest that IL-17 inhibition can ameliorate SLE by inhibiting B- cell differentiation into GCs. Therefore, IL-17-producing Th17 cells show promise as a target for development of novel therapeutics for SLE.
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