Abstract: TH-PO545
HMGB1 and Antiphospholipid Antibodies Are Involved in the Pathogenesis of Systemic Lupus Erythematosus
Session Information
- Pathology and Lab Medicine
November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1700 Pathology and Lab Medicine
Authors
- Guan, Hui, Department of Nephrology, Center of Kidney and Urology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China
- Wang, Xiaohua, Department of Nephrology, Center of Kidney and Urology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China
- Tang, Chun, Department of Nephrology, Center of Kidney and Urology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China
- Wu, Keping, Department of Nephrology, Center of Kidney and Urology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China
- Chen, Jiasi, Department of Nephrology, Center of Kidney and Urology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China
- Zheng, Zhihua, Department of Nephrology, Center of Kidney and Urology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China
Background
Antiphospholipid antibodies (aPLs） are involved in the multiorgan damage of systemic lupus erythematosus (SLE). High Mobility Group Protein 1(HMGB1) can promote the secretion of antuantibodies in SLE. The study aims to explore the role of HMGB1 and aPLs in the pathogenesis of lupus nephritis.
Methods
Antiphospholipid antibodies and HMGB1 levels were detected by enzyme-linked immunosorbent assays. Enzyme-linked immunospot assay was used to detect the ability of B cells to secrete antibodies.
Results
Anti-phosphatidylserine (PS) antibodies were significantly different between the SLE and control groups, while anti-phosphatidylserine/prothrombin (PS/PT) and anti-prothrombin (PT) were not. Anti-PS IgG antibodies were positively correlated to disease activity in SLE patients, while others were not. HMGB1 of SLE patients was correlated with anti-PS antibodies. HMGB1 protein stimulated peritoneal B-1a cells of C57 mice to secrete anti-PS IgG antibodies, which could not be blocked by TLR4 inhibitors (CLI-095).
Conclusion
Anti-PS antibodies and HMGB1 are involved in the pathogenesis of SLE.
Comparison of antiphospholipid antibodies between healthy controls and SLE patients.
Antiphospholipid antibodies and HMGB1 were involved in the pathogenesis of SLE.