Specific Inhibition of Soluble gamma c Receptor Attenuates Collagen-Induced Arthritis by Modulating the Inflammatory T Cell Responses
SCIE
SCOPUS
- Title
- Specific Inhibition of Soluble gamma c Receptor Attenuates Collagen-Induced Arthritis by Modulating the Inflammatory T Cell Responses
- Authors
- Lee, Byunghyuk; Jo, Yuna; Kim, Geona; Ali, Laraib Amir; Sohn, Dong Hyun; Lee, Seung-Geun; Kim, Kiseok; Shin, Euisu; Ryu, Sung Ho; Hong, Changwan
- Date Issued
- 2019-02
- Publisher
- FRONTIERS MEDIA SA
- Abstract
- IL-17 produced by Th17 cells has been implicated in the pathogenesis of rheumatoid arthritis (RA). It is important to prevent the differentiation of Th17 cells in RA. Homodimeric soluble gamma c (s gamma c) impairs IL-2 signaling and enhances Th17 differentiation. Thus, we aimed to block the functions of s gamma c by inhibiting the formation of homodimeric s gamma c. The homodimeric form of s gamma c was strikingly disturbed by s gamma c-binding DNA aptamer. Moreover, the aptamer effectively inhibited Th17 cell differentiation and restored IL-2 and IL-15 signaling impaired by s gamma c with evidences of increased survival of T cells. s gamma c was highly expressed in SF of RA patients and increased in established CIA mice. The therapeutic effect of PEG-aptamer was tested in CIA model and its treatment alleviated arthritis pathogenesis with impaired differentiation of pathogenic Th17, NKT1, and NKT17 cells in inflamed joint. Homodimeric s gamma c has pathogenic roles to exacerbate RA progression with differentiation of local Th17, NKT1, and NKT17 cells. Therefore, s gamma c is suggested as target of a therapeutic strategy for RA.
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/100070
- DOI
- 10.3389/fimmu.2019.00209
- ISSN
- 1664-3224
- Article Type
- Article
- Citation
- FRONTIERS IN IMMUNOLOGY, vol. 10, page. 209, 2019-02
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