Autoimmune diseases can be chronic with relapse of inflammatory symptoms, but it can be also acute and life-threatening if immune cells destroy life-supporting organs, such as lupus nephritis. The etiopathogenesis of autoimmune diseases has been revealed as that genetics and environmental factors-mediated dysregulated immune responses contribute to the initiation and development of autoimmune disorders. However, the current understanding of pathogenesis is limited and the underlying mechanism has not been well defined, which lows the development of novel biomarkers and new therapeutic strategies for autoimmune diseases. To improve this, broadening and deepening our understanding of pathogenesis is an unmet need. As genetic susceptibility cannot explain the low accordance rate of incidence in homozygous twins, epigenetic regulations might be an additional explanation. Therefore, this review will summarize current progress of studies on epigenetic dysregulations contributing to autoimmune diseases, including SLE, rheumatoid arthritis (RA), psoriasis, type 1 diabetes (T1D), and systemic sclerosis (SSc), hopefully providing opinions on orientation of future research, as well as discussing the clinical utilization of potential biomarkers and therapeutic strategies for these diseases.

Absent in melanoma 2 (AIM2) is a novel member of interferon (IFN)‐inducible PYHIN proteins. In innate immune cells, AIM2 servers as a cytoplasmic double‐stranded DNA sensor, playing a crucial role in the initiation of the innate immune response as a component of the inflammasome. AIM2 expression is increased in patients with systemic lupus erythematosus (SLE), psoriasis, and primary Sjogren's syndrome, indicating that AIM2 might be involved in the pathogenesis of autoimmune diseases. Meanwhile, AIM2 also plays an antitumorigenesis role in an inflammasome independent‐manner. In melanoma, AIM2 is initially identified as a tumor suppressor factor. However, AIM2 is also found to contribute to lung tumorigenesis via the inflammasome‐dependent release of interleukin 1β and regulation of mitochondrial dynamics. Additionally, AIM2 reciprocally dampening the cGAS‐STING pathway causes immunosuppression of macrophages and evasion of antitumor immunity during antibody treatment. To summarize the complicated effect and role of AIM2 in autoimmune diseases and cancers, herein, we provide an overview of the emerging research progress on the function and regulatory pathway of AIM2 in innate and adaptive immune cells, as well as tumor cells, and discuss its pathogenic role in autoimmune diseases, such as SLE, psoriasis, primary Sjogren's syndrome, and cancers, such as melanomas, non‐small‐cell lung cancer, colon cancer, hepatocellular carcinoma, renal carcinoma, and so on, hopefully providing potential therapeutic and diagnostic strategies for clinical use.

BackgroundNeonatal sepsis is an inflammatory systemic syndrome, which is a major cause of morbidity and mortality in premature infants. We analyzed the expression profile data of E-MTAB-4785 to reveal the pathogenesis of the disease.MethodsThe expression profile dataset E-MTAB-4785, which contained 17 sepsis samples and 19 normal samples, was obtained from the ArrayExpress database. The differentially expressed genes (DEGs) were analyzed by the Bayesian testing method in limma package. Based on the DAVID online tool, enrichment analysis was conducted for the DEGs. Using STRING database and Cytoscape software, protein-protein interaction (PPI) network and module analyses were performed. Besides, transcription factor (TF)-DEG regulatory network was also constructed by Cytoscape software. Additionally, miRNA-DEG pairs were searched using miR2Disease and miRWalk 2.0 databases, followed by miRNA-DEG regulatory network was visualized by Cytoscape software.ResultsA total of 275 DEGs were identified from the sepsis samples in comparison to normal samples. TSPO, MAPK14, and ZAP70 were the hub nodes in the PPI network. Pathway enrichment analysis indicated that CEBPB and MAPK14 were enriched in TNF signaling pathway. Moreover, CEBPB and has-miR-150 might function in neonatal sepsis separately through targeting MAPK14 and BCL11B in the regulatory networks. These genes and miRNA might be novel targets for the clinical treatment of neonatal sepsis.ConclusionTSPO, ZAP70, CEBPB targeting MAPK14, has-miR-150 targeting BCL11B might affect the pathogenesis of neonatal sepsis. However, their roles in neonatal sepsis still needed to be confirmed by further experimental researches.

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