ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 1614

The Impact of High Risk Susceptible Gene  LILRA3  on Joint Inflammation in Rheumatoid Arthritis

Mengru Liu1, Yan Du2, Jing Zhang1, Fanlei Hu1, Li Zheng3, Yingni Li3, Jianping Guo1 and Z. Li1, 1Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing, China, 2Department of Rheumatology and Immunology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang, China, 3Peking University People's Hospital, Beijing, China

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords:

Session Information

Date: Monday, November 9, 2015

Title: Rheumatoid Arthritis - Human Etiology and Pathogenesis Poster II

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose: Leukocyte immunoglobulin-like receptor A3 (LILRA3) is a putatively secreted protein belongs to the leukocyte immunoglobulin-like receptor (LILR) family. Based on our research that LILRA3 is a novel genetic risk for rheumatoid arthritis (RA) in Chinese Han population , we undertake this study to investigate the role of LILRA3 on synovium inflammation  in RA patients.

Methods:  i) The expression of LILRA3 in serum and synovial fluid from patients with RA ,OA, and health controls were measured by using ELISA. ii) Fibroblast-like synoviocytes (FLSs) from RA patients were stimulated with different concentration of recombinant LILRA3 protein in the presence or absence of tumour necrosis factor (TNF)-α and interleukin (IL)-1β. iii) FLSs from patients with RA were transfected with LILRA3 plasmid or control vector and 24 hours later were treated with TNF-α and IL-1β co-culture. The expression of inflammatory mediators, including IL-6,IL-8, MMP-1and MMP-3 was measured by q-PCR array and ELISA. MARKinse signaling pathway activation levels were detected by Western Blotting method. One-way analysis of variance was used to detect the differences between the group means.

Results: Compared with health controls, the expression of LILRA3 in RA and OA serum was high and LILRA3 was specifically express in synovial fluid with RA patients. We demonstrated that LILRA3 can promote the secretion of inflammatory factors independently or synergy with TNF-α and IL-1β both in vitro and in a transfect system. Furthermore, we proved that LILRA3 can promoted synovium inflammation through the activation of the signaling pathways, particularly the ERK and JNK pathways.

Conclusion:

Our data demonstrate that LILRA3 is a potent new pro-inflammatory factor in RA. LILRA3 can aggravates synovium inflammation through MARKinse signaling pathway. These findings may give us some clues for the study on the pathogenesis of RA.

Disclosure: M. Liu, None; Y. Du, None; J. Zhang, None; F. Hu, None; L. Zheng, None; Y. Li, None; J. Guo, None; Z. Li, None.

To cite this abstract in AMA style:

Liu M, Du Y, Zhang J, Hu F, Zheng L, Li Y, Guo J, Li Z. The Impact of High Risk Susceptible Gene  LILRA3  on Joint Inflammation in Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/the-impact-of-high-risk-susceptible-gene-lilra3-on-joint-inflammation-in-rheumatoid-arthritis/. Accessed .

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