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Abstract
Lupus nephritis (LN) is an immune complex-mediated inflammatory renal manifestation and one of the most serious complications of systemic lupus erythematosus. Clinical diagnosis of LN mainly relies on renal biopsy, and it is one of the main causes of end-stage renal disease. In the process of LN, abnormal apoptosis of cells is accompanied by the failure of apoptosis products, leading to the constant exposure of antigens, continuous activation of immune responses, and production of antibodies. The pathogenesis of this disease remains unclear. Genetic defects, epigenetic modification anomalies, and environmental factors are the common etiology of the disease. HMGB1 is a nuclear protein that binds to DNA and acts as an architectural chromatin-binding factor. It can also be released from cells, and the extracellular form binds the inflammatory receptor for advanced glycation end-products (RAGE) and Toll-like receptors (TLRs). In this paper, the pathogenesis of LN is discussed from the perspective of natural and acquired immunity, and the roles of HMGB1, TLRs, and the HMGB1/TLR4 pathway in the pathogenesis of LN are analyzed with the aim of proposing new ideas for treatment improvement.
Am J Transl Med 2023. 7(2): 78-85