Immune‐related genes (IRGs) have been identified as critical drivers of the initiation and progression of hepatocellular carcinoma (HCC). This study is aimed at constructing an IRG signature for HCC and validating its prognostic value in clinical application. The prognostic signature was developed by integrating multiple IRG expression data sets from TCGA and GEO databases. The IRGs were then combined with clinical features to validate the robustness of the prognostic signature through bioinformatics tools. A total of 1039 IRGs were identified in the 657 HCC samples. Subsequently, the IRGs were subjected to univariate Cox regression and LASSO Cox regression analyses in the training set to construct an IRG signature comprising nine immune‐related gene pairs (IRGPs). Functional analyses revealed that the nine IRGPs were associated with tumor immune mechanisms, including cell proliferation, cell‐mediated immunity, and tumorigenesis signal pathway. Concerning the overall survival rate, the IRGPs distinctly grouped the HCC samples into the high‐ and low‐risk groups. Also, we found that the risk score based on nine IRGPs was related to clinical and pathologic factors and remained a valid independent prognostic signature after adjusting for tumor TNM, grade, and grade in multivariate Cox regression analyses. The prognostic value of the nine IRGPs was further validated by forest and nomogram plots, which revealed that it was superior to the tumor TNM, grade, and stage. Our findings suggest that the nine‐IRGP signature can be effective in determining the disease outcomes of HCC patients.

Background: Asthma and cardiovascular disease (CVD) share many risk factors. Previous meta-analyses indicated that asthma is associated with an increased risk of CVD and all-cause mortality, but these studies were limited by unstandardized search strategies and the number of articles included. Objective: We sought to systematically synthesize evidence investigating the impact of asthma on all-cause mortality and CVD morbidity and mortality. Methods: We searched in PubMed and EMBASE for observational cohort studies (inception dates to November 10, 2021) that had both asthma groups and control groups. We also manually searched the reference lists of correlative articles to include other eligible studies. Data for associations between asthma and all-cause mortality and CVD morbidity and mortality were needed. Results: We summarized the findings from 30 cohort studies comprising 4,157,823 participants. Asthma patients had increased CVD morbidity [relative risk (RR) = 1.28, 95% confidence interval (CI) = 1.16–1.40] and increased CVD mortality (RR = 1.25, 95% CI = 1.14–1.38). Asthma patients also had increased risk of all-cause mortality (RR = 1.38, 95% CI = 1.07–1.77). In subgroup analyses, female asthma patients had a higher risk of CVD morbidity and all-cause mortality than male asthma patients, and late-onset asthma patients had a higher risk of CVD morbidity than early-onset asthma patients. Conclusion: Asthma patients have increased risk of all-cause mortality and CVD morbidity and mortality. This information reminds clinicians to be aware of the risk of CVD and all-cause mortality in asthma patients. Systematic Review Registration: http://www.crd.york.ac.uk/PROSPERO/, PROSPERO, identifier: CRD 42021290082.

Interleukin (IL)-33 is a member of the IL-1 superfamily and is a crucial cytokine playing the role of a dual-function molecule. IL-33 mediates its function by interacting with its receptor suppression of tumorigenicity 2 (ST2), which is constitutively expressed on T helper (Th)1 cells, Th2 cells, and other immune cells. Previously, we summarized findings on IL-33 and performed an intensive study of the correlation between IL-33 and tumor. IL-33 enables anti-tumor immune responses through Th1 cells and natural killer (NK) cells and plays a role in tumor immune escape in cancers via Th2 cells and regulatory T cells. Herein, we discuss the contradictory role of IL-33 in immune cells in different cancer, and our summaries may be helpful for better understanding of the development of research on IL-33 and tumor immunity.

Background: Cancer-associated fibroblasts (CAFs) are essential stromal components in the tumor microenvironment of hepatocellular carcinoma (HCC). Hepatitis B virus (HBV) infection induces pathological changes such as liver fibrosis/cirrhosis and HCC. The aim of this research was to explore the novel mediators of CAFs to modulate HBV cirrhosis-HCC progression. Methods: The single-cell transcriptome data of HCC were divided into subsets, and the significant subset related to fibrotic cells, along with biological function, and clinical information of HCC was revealed by integrated data analyses. The cell communication, cells communicated weight analysis of signaling pathways, and key genes in signaling pathways analysis of significant CAFs subclasses were conducted to discover the novel gene of CAFs. Bioinformatics, vitro and HBV transfection assays were used to verify the novel gene is an important target for promoting the progression HBV cirrhosis-HCC progression. Results: Fibroblasts derived from HCC single-cell data could be separated into three cell subclasses (CAF0-2), of which CAF2 was associated with the HCC clinical information. Fibroblasts have opposite developmental trajectories to immune B cells and CD8 + T cells. CAF0-2 had strong interaction with B cells and CD8 + T cells, especially CAF2 had the highest interaction frequency and weight with B cells and CD8 + T cells. Moreover, PTN participated in CAF2-related pathways involved in the regulation of cell communication, and the interactions among CAF2 and PTN contributed the most to B cells and CD8 + T cells. Furthermore, the genes of PTN, SDC1, and NCL from PTN signaling were highest expression in CAF2, B cells, and CD8 + T cells, respectively, and the interaction of PTN- SDC1 and PTN- NCL contributed most to the interaction of CAF2- B cells and CAF2-CD8 + T cells. Bioinformatics and vitro experiments confirm PTN was upregulated in HCC and promoted the proliferation of tumor cells, and HBV infection could initiate PTN to perform cirrhosis-HCC progression. Conclusion: Our findings revealed CAF was associated with hepatocarcinogenesis, and the functional importance of B cells and CD8 + T cells in modulating CAF in HCC. Importantly, PTN maybe a novel mediator of CAF to mediate HBV cirrhosis-HCC progression.

Aim: This study aimed to identify long noncoding RNAs (lncRNAs) with potential to be prognostic biomarkers of hepatocellular carcinoma (HCC) by analyzing copy number alterations (CNAs). Methods: RN...

In this study, we explored the genes genetically associated with lupus nephritis (LN), and their function by bioinformatics analysis. We collected genes potentially associated with LN from National Center for Biotechnology Information Center (NCBI-Gene) and Online Mendelian Inheritance in Man (OMIM) databases. The major bioinformatics analysis linked with genes was then revealed by weighted gene co-expression network analysis (WGCNA), crosstalk analysis, functional analysis, and Pivot algorithm. Two hundred twenty-three LN-related genes were obtained by intersecting NCBI-Gene and OMIM databases. Two thousand five hundred sixty-eight LN-related proteins and 23 modules were excavated by String protein interaction network and WGCNA co-expression analysis, respectively. Pivot algorithm included no coding RNA, transcription factor and drug indicated the high-count correlation-associated modules related to cancer, kidney pathophysiological changes, and kidney injury, respectively. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis based on 23 modules revealed LN-related genes mainly involved in immune response. Moreover, 19 genes that came from intersection of LN, arthritis, pleurisy, and myocarditis have close relationship with immune diseases and immune processes. Our results from this research may have important implications for understanding the genes underlying LN. Also, the framework proposed in this work can be used to research pathological molecular network and genes related to LN.