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Updated: Dec 18, 2025

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
Published on: November 1, 2015
HMGB1 in Systemic Lupus Erythematosus
Tianye Liu1,2, Myoungsun Son1,2, Betty Diamond1,2
1Center for Autoimmune Musculoskeletal and Hematopoietic Diseases, Institute of Molecular Medicine, The Feinstein Institutes for Medical Research, Manhasset, NY, United States.
High-mobility group box 1 (HMGB1) drives inflammation in Systemic Lupus Erythematosus (SLE). Understanding HMGB1
Area of Science:
- Immunology
- Molecular Biology
- Rheumatology
Background:
- High-mobility group box 1 (HMGB1) is a nuclear protein with potent proinflammatory effects on innate immune cells.
- Extracellular HMGB1 acts as a damage-associated molecular pattern (DAMP), mediating inflammation during cellular damage.
- Systemic Lupus Erythematosus (SLE) is characterized by chronic inflammation and autoantibody production.
Purpose of the Study:
- To elucidate the role and properties of HMGB1 in the pathogenesis of Systemic Lupus Erythematosus (SLE).
- To explore HMGB1's contribution to SLE disease phenotypes and inflammation.
- To identify potential therapeutic targets for SLE based on HMGB1 activity.
Main Methods:
- Review and analysis of existing literature on HMGB1 function in innate immunity and SLE.
- Examination of HMGB1's role as a DAMP in the context of impaired apoptotic debris clearance in SLE patients.
- Correlation of HMGB1 activity with specific SLE manifestations like lupus nephritis and neuropsychiatric lupus.
Main Results:
- HMGB1 is released extracellularly in SLE due to impaired clearance of apoptotic cells.
- Extracellular HMGB1 contributes significantly to the non-resolving inflammation characteristic of SLE.
- HMGB1 is implicated in diverse SLE phenotypes, including lupus nephritis and neuropsychiatric lupus.
Conclusions:
- HMGB1 plays a critical role in driving inflammation and disease progression in Systemic Lupus Erythematosus.
- Targeting HMGB1 presents a promising therapeutic strategy for managing SLE and its associated complications.
- Further research into HMGB1's mechanisms in SLE can lead to novel treatment opportunities.
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