The global population is aging at a rapid pace. By 2050, the number of people aged 60 and above is expected to soar to two billion, up from 800 million in 2011, with around 80% residing in lower-income nations [1]. At the same time, the number of older individuals (those 50 and older [2,3]) living […]

Background: Systemic lupus erythematosus (SLE) is a complex heterogeneous systemic autoimmune disease. Previous studies have shown that SLE may be related to diffuse large B cell lymphoma (DLBCL), but the mechanism of their relationship is still unclear. The present study aimed to explore the common genetic molecular mechanisms, core shared genes, and miRNAs between SLE and DLBCL as well as to investigate the diagnostic markers of DLBCL. Methods: The SLE and DLBCL microarray data were downloaded from the comprehensive Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was used to identify co-expression modules. Four core shared genes were screened out by various algorithms and validated in other cohorts. Finally, we constructed a common core gene-miRNA network using the human microRNA disease database (HMDD) and TarBase. Results: Using WGCNA, four modules were identified as important modules for SLE and DLBCL. Enrichment analysis of the shared genes showed that the highly activated NF-κB pathway was a common feature of the pathophysiology. Four core shared genes, namely, PSMB10, PSMB4, TAF10, and NFΚBIA, were screened out. These core shared genes were significantly upregulated in both diseases, and they may be potential diagnostic markers of DLBCL. The core gene-miRNA network showed that miR-155–5p, regulating the shared NF-κB pathway, may play an important role in the susceptibility of SLE patients to DLBCL. Conclusion: The present study revealed that NF-κB pathway in SLE may be a crucial susceptible factor for DLBCL. In addition, we identified PSMB10, PSMB4, TAF10, NFΚBIA and miR-155 involved in the common pathogenesis as potential biomarkers and therapeutic targets for DLBCL.

Immune-mediated inflammatory diseases (IMIDs) are chronic inflammatory diseases caused by immune system dysregulation, affecting multiple systems and organs. Children and adolescents aged 10-24 are among the high-risk groups, and the global burden is substantial. Using the latest data from global burden of disease (GBD) 2021, we employed Joinpoint regression analysis, Socio-Demographic Index (SDI) correlation analysis, and cross-national equity analysis to elucidate the spatiotemporal differences in the burden of IMIDs among 10-24-year-olds from 1990 to 2021. The burden of IMIDs in adolescents aged 10-24, ranked by severity, includes asthma, atopic dermatitis (AD), psoriasis, diabetes, rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and multiple sclerosis (MS). Among these, asthma, AD, psoriasis, RA, and MS are more prevalent in females. Compared to 1990, the incidence rates of asthma and AD decreased in 2021, while the rates of psoriasis, diabetes, and RA increased. IMIDs are more common in Western Europe and North America, with rising incidence rates in South America and Asia. Concentration indices and slope indices indicate that these diseases are primarily concentrated in high SDI regions, although the differences in incidence rates between countries are decreasing. While focusing on high-incidence regions, we must also pay attention to the incidence of IMIDs in emerging regions such as Asia and South America. Only in this way can we effectively reduce the heavy burden that IMIDs place on younger people globally.