Yaxuan Deng

Abstract Large-scale COVID-19 vaccinations are currently underway in many countries in response to the COVID-19 pandemic. Here, we report, besides generation of neutralizing antibodies, consistent alterations in hemoglobin A1c, serum sodium and potassium levels, coagulation profiles, and renal functions in healthy volunteers after vaccination with an inactivated SARS-CoV-2 vaccine. Similar changes had also been reported in COVID-19 patients, suggesting that vaccination mimicked an infection. Single-cell mRNA sequencing (scRNA-seq) of peripheral blood mononuclear cells (PBMCs) before and 28 days after the first inoculation also revealed consistent alterations in gene expression of many different immune cell types. Reduction of CD8 + T cells and increase in classic monocyte contents were exemplary. Moreover, scRNA-seq revealed increased NF-κB signaling and reduced type I interferon responses, which were confirmed by biological assays and also had been reported to occur after SARS-CoV-2 infection with aggravating symptoms. Altogether, our study recommends additional caution when vaccinating people with pre-existing clinical conditions, including diabetes, electrolyte imbalances, renal dysfunction, and coagulation disorders.

Background Systemic lupus erythematosus (SLE) and primary Sjögren’s syndrome (pSS) are common systemic autoimmune diseases that share a wide range of clinical manifestations and serological features. This study investigates genes, signaling pathways, and transcription factors (TFs) shared between SLE and pSS. Methods Gene expression profiles of SLE and pSS were obtained from the Gene Expression Omnibus (GEO). Weighted gene co-expression network analysis (WGCNA) and differentially expressed gene (DEG) analysis were conducted to identify shared genes related to SLE and pSS. Overlapping genes were then subject to Gene Ontology (GO) and protein-protein interaction (PPI) network analyses. Cytoscape plugins cytoHubba and iRegulon were subsequently used to screen shared hub genes and predict TFs. In addition, gene set variation analysis (GSVA) and CIBERSORTx were used to calculate the correlations between hub genes and immune cells as well as related pathways. To confirm these results, hub genes and TFs were verified in microarray and single-cell RNA sequencing (scRNA-seq) datasets. Results Following WGCNA and limma analysis, 152 shared genes were identified. These genes were involved in interferon (IFN) response and cytokine-mediated signaling pathway. Moreover, we screened six shared genes, namely IFI44L, ISG15, IFIT1, USP18, RSAD2 and ITGB2 , out of which three genes, namely IFI44L, ISG15 and ITGB2 were found to be highly expressed in both microarray and scRNA-seq datasets. IFN response and ITGB2 signaling pathway were identified as potentially relevant pathways. In addition, STAT1 and IRF7 were identified as common TFs in both diseases. Conclusion This study revealed IFI44L, ISG15 and ITGB2 as the shared genes and identified STAT1 and IRF7 as the common TFs of SLE and pSS. Notably, the IFN response and ITGB2 signaling pathway played vital roles in both diseases. Our study revealed common pathogenetic characteristics of SLE and pSS. The particular roles of these pivotal genes and mutually overlapping pathways may provide a basis for further mechanistic research.

Neural repair within the central nervous system (CNS) has been extremely challenging due to limited abilities of adult CNS neurons to regenerate, particularly in a highly inflammatory injury environment that is also filled with myelin debris. Spinal cord injury (SCI) is a serious medical condition that often leads to paralysis and currently has no effective treatment. Here we report the construction of a novel biocompatible and biodegradable material, Bio-C, through coating of acid-desalted-collagen (ADC) tube with pre-modified hyaluronic acid, which, after implantation, can elicit quite robust neural regeneration and functional recovery after complete spinal-cord transection with a 2 mm-spinal-cord-segment removal in mice. We combined morphological, electrophysiological, and objective transcriptomic analyses, in addition to behavioral analyses, to demonstrate neural tissue regeneration and functional recovery through the establishment of Bio-C-induced anti-inflammatory, neurogenic, and neurotrophic microenvironment. Through this study, we unveiled the underlying logic for CNS neural repair.

Exploring the shared molecular mechanisms between systemic lupus erythematosus and primary Sjögren's syndrome based on integrated bioinformatics and single-cell RNA-seq analysis By Cui Y, Zhang H, Wang Z, Gong B, Al-Ward H, Deng Y, Fan O, Wang J, Zhu W andSun YE (2023). Front. Immunol. 14:1212330. doi: 10.3389/fimmu.2023.1212330.In the published article, there was an error in Figures 8C, 9A, 9B, 10C, 10E, S5E, S6A, S7E as published. We noticed that a cell type was incorrectly described. The "gd T cells" should be "CD8 memory T cells" in our article since the R codes were not revised in time. The corrected Figures 8C, 9A, 9B, 10C, 10E, S5E

BACKGROUND: Mixed connective tissue disease (MCTD) is a rare autoimmune disease, and little is known about its pathogenesis. Furthermore, MCTD, systemic lupus erythematosus (SLE), and primary Sjögren's syndrome (pSS) share many clinical, laboratory, and immunological manifestations. This overlap complicates early diagnosis and accurate treatment. METHODS: The transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) from MCTD patients was performed using both bulk RNA sequencing and single-cell RNA sequencing (scRNA-seq) for the first time. Additionally, we applied MCTD scRNA-seq data, along with datasets from SLE (GSE135779) and pSS (GSE157278) from the Gene Expression Omnibus database, to characterize and compare the similarities and heterogeneity among MCTD, SLE, and pSS. RESULTS: effector T cells was increased, while mucosal-associated invariant T cells were decreased in all three diseases. Genes related to the 'interferon (IFN) γ response' and 'IFN α response' were significantly upregulated. SCENIC analysis revealed activation of STAT1 and IRF7 in disease states, targeting IFN-related genes. The IFN-II signaling network was notably elevated in all three diseases. Unique features of MCTD, SLE, and pSS were also identified. CONCLUSION: We dissected the immune landscape of MCTD at single-cell resolution, providing new insights into the development of novel biomarkers and immunotherapies for MCTD. Furthermore, we offer insights into the transcriptomic similarities and heterogeneity across different autoimmune diseases, while highlighting prospective therapeutic targets.