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Abstract Number: 1185

Interleukin-11 Promotes Fibrosis Through Classic and Trans-signaling Pathway in Systemic Sclerosis

Wenjing Ye1, Qian Wang1, Li Zhao2, Changcheng Wang3, Dandan Zhang4, Mengyu Zhou4, Fangfang Chen2, Zaihua Zhu2, Weiguo Wang2, Wenyu Guo5, Yun Liu4, Hejian Zou2 and Yu Xue2, 1epartment of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China, 2Department of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China, 3Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China, 4MOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, China, 5Clinical Development, I-Mab Biopharma (Hangzhou) Co., Ltd, Shanghai, China

Meeting: ACR Convergence 2022

Keywords: Fibroblasts, Dermal, Interleukins, Systemic sclerosis

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Session Information

Date: Sunday, November 13, 2022

Title: Systemic Sclerosis and Related Disorders – Basic Science Poster

Session Type: Poster Session C

Session Time: 1:00PM-3:00PM

Background/Purpose: Interleukin-11 (IL-11) was found significantly upregulated in Systemic sclerosis (SSc), the aim of this study is to explore the pathological role of IL-11 and clarify the potential therapeutic value of targeting IL-11 in SSc.

Methods: Plasma IL-11 level was tested by ELISA, and the expression of ADAM10, IL-11 and IL-11Rα in skin were measured by immunohistochemistry. RNA-Seq was performed to analyze the transcription change in IL-11 overexpressing fibroblast cells. Soluble IL-11Rα (sIL-11Rα) induced by ionomycin (iono) was used to evaluate the pro-fibrotic effect of IL-11 trans-signaling pathway in fibroblast. TJ301(sgp130Fc, an inhibitor of IL-11 trans-signaling) intervention group was set up to investigate the anti-fibrosis effect of targeting IL-11 trans-signaling pathway in both cellular and animal experiments. Meanwhile, WP1066 was used to block STAT3 pathway in cellular study.

Results: Plasma IL-11 level was extremely low in most SSc patients and healthy controls, while IL-11, IL-11Rα and ADAM10 were significantly elevated in skin samples of SSc patients. RNA-Seq analysis displayed some fibrotic-related genes were dysregulated in IL-11 overexpressing cells, and differentially expressed genes (DEGs) were enriched in TGF-β effect and collagen metabolism pathway. Fibroblasts stimulated with IL-11 with iono could induce COL3 expression and STAT3 phosphorylation, and the pro-fibrotic effect could be inhibited by TJ301 or WP1066. TJ301 also ameliorated skin and lung fibrosis in BLM induced-SSc mice.

Conclusion: Besides classic signaling pathway, IL-11 contributes to pro-fibrosis in SSc through regulating trans-signaling pathway. Intervention of IL-11 trans-signaling pathway or JAK2/STAT3 pathway could ameliorate the pro-fibrotic response of IL-11.

Supporting image 1

Figure. Pro-fibrotic effect of IL_11.


Disclosures: W. Ye, None; Q. Wang, None; L. Zhao, None; C. Wang, None; D. Zhang, None; M. Zhou, None; F. Chen, None; Z. Zhu, None; W. Wang, None; W. Guo, None; Y. Liu, None; H. Zou, None; Y. Xue, None.

To cite this abstract in AMA style:

Ye W, Wang Q, Zhao L, Wang C, Zhang D, Zhou M, Chen F, Zhu Z, Wang W, Guo W, Liu Y, Zou H, Xue Y. Interleukin-11 Promotes Fibrosis Through Classic and Trans-signaling Pathway in Systemic Sclerosis [abstract]. Arthritis Rheumatol. 2022; 74 (suppl 9). https://acrabstracts.org/abstract/interleukin-11-promotes-fibrosis-through-classic-and-trans-signaling-pathway-in-systemic-sclerosis/. Accessed .
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