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Moderate-to-severe systemic lupus erythematosus (SLE) is characterized by extensive autoantibody deposition and persistent autoinflammation. As the existing animal models are limited in accurately reproducing the pathological characteristics of human SLE, we introduced a novel animal model simulating multi-organ autoinflammation through intra-organ injections. The model closely mimicked key features of SLE, including IgG deposition, inflammation, and tissue damage. The model could be used to assess the roles of IgG, immune cells, cytokines, and Fc gamma receptor (FcγR) in the pathogenesis of autoinflammation. The results obtained from this model could be confirmed by lupus MRL/ lpr mice. The review suggested that the diagnostic criteria should be reconsidered to incorporate IgG deposition in tissues and highlighted the limitations of current T-cell and B-cell-focused treatments. To summarize, the IgG deposition model can be used to investigate the pathogenesis and treatment of multi-organ tissue damage associated with SLE. • Introduction of a novel animal model: a new animal model mimicing the pathogenesis of lupus autoantibodies IgG-induced organ-tissue damage. • Comprehensive Exploration and Validation of New Model: The roles of lupus autoantibody IgG, immune cells, cytokines and FcγR in organ tissue inflammation were investigated by using this new model. Confirmation of the results from the new model using lupus-prone MRL/lpr mice. • Implications for SLE Research and Treatment: Importance and convenience of the IgG deposition model in investigating the pathogenesis of SLE and its potential for developing targeted therapies. • This paper significantly contributes to the understanding of SLE pathogenesis by introducing a novel animal model that accurately replicates key aspects of the disease, providing a platform for more effective therapeutic exploration and diagnostic considerations. [ABSTRACT FROM AUTHOR]

Ischemic stroke (IS) is a significant global public health issue with a high incidence, disability, and mortality rate. A robust inflammatory cascade with complex and wide-ranging mechanisms occurs following ischemic brain injury. Inflammasomes are multiprotein complexes in the cytoplasm that modulate the inflammatory response by releasing pro-inflammatory cytokines and inducing cellular pyroptosis. Among these inflammasomes, the Absent in Melanoma 2 (AIM2) inflammasome shows the ability to detect a wide range of pathogen DNAs, thereby triggering an inflammatory response. Recent studies have indicated that the aberrant expression of AIM2 inflammasome in various cells is closely associated with the pathological processes of ischemic brain injury. This paper summarizes the expression and regulatory role of AIM2 in CNS and peripheral immune cells and discusses current therapeutic approaches targeting AIM2 inflammasome. These findings aim to serve as a reference for future research in this field. • The AIM2 inflammasomes are regarded as the key participants in the inflammatory response following ischemic stroke. • The pathological progression of ischemic brain injury involves aberrant expression of AIM2 inflammasomes in various cells. • Specific inhibitors directed towards AIM2 inflammasomes have the potential to serve as therapeutic agents for the management of neurological damage following an ischemic stroke [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is a typical systemic autoimmune disease that manifests as skin rash, arthritis, lymphadenopathy, and multiple organ lesions. Epigenetics, including DNA methylation, histone modification, and non-coding RNA regulation, mainly affect the function and characteristics of cells through the regulation of gene transcription or translation. Increasing evidence indicates that there are a variety of complex epigenetic effects in patients with SLE, which interfere with the differentiation and function of T, and B lymphocytes, monocytes, and neutrophils, and enhance the expression of SLE-associated pathogenic genes. This paper summarizes our currently knowledge regarding pathogenesis of SLE, and introduces current advances in the epigenetic regulation of SLE from three aspects: immune function, inflammatory response, and lupus complications. We propose that epigenetic changes could be used as potential biomarkers and therapeutic targets of SLE. • Epigenetic modifications are widely involved in the pathogenesis of SLE. • Epigenetic modifications promote and maintain continuous immune activation and chronic inflammation. • Epigenetic modifications promote and maintain continuous immune activation and chronic inflammation. [ABSTRACT FROM AUTHOR]