Abstract
High-mobility group box 1 (HMGB1) is an important molecule for several nuclear processes. Recently, HMGB1 has gained much attention as a damage-associated molecular pattern (DAMP) and has been implicated in the pathogenesis of several (auto)-immune diseases, in particular, systemic lupus erythematosus (SLE). A main pathogenic feature in SLE is the accumulation of apoptotic cells. Since HMGB1 is released from apoptotic cells it has been hypothesized that HMGB1 might fuel the inflammatory processes, as seen in this disease, and play a fundamental role in the pathogenesis. In this review, we discuss evidence in support of the theory that HMGB1 is an important mediator in SLE and may be considered a new autoantigen.
Highlights
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease, characterized by the involvement of many organs and the presence of autoantibodies directed to nuclear and cytoplasmic antigens
The data in this study are in line with the results found by Urbonaviciute et al [30], who showed that injecting HMGB1nucleosome complexes induced antidsDNA production through TLR2 in
receptor for advanced glycation end products (RAGE), vascular cell adhesion molecule (VCAM)-1 and inducible cell adhesion molecule (ICAM)-1 showed higher expression on the cell surface. These effects could be blocked by adding box A or soluble RAGE, indicating that High-mobility group box 1 (HMGB1) plays an important role in mediating inflammation in endothelial cells
Summary
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease, characterized by the involvement of many organs and the presence of autoantibodies directed to nuclear and cytoplasmic antigens. They showed that a monoclonal antibody to HMGB1 significantly reduced interferon (IFN)-α production in peripheral blood mononucleated cells stimulated with plasma from lupus patients containing HMGB1-CpG complexes [29]. They showed that stimulating endothelial cells with immune complexes from SLE patients increased proinflammatory cytokines such as IL-6 and IL-8.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
