Rheumatoid arthritis (RA) is associated with a high rate of hepatitis B virus (HBV) infection. A large proportion of HBV reactivation may occur in RA patients after immunosuppression treatment, while fulminant hepatitis may occur in severe cases. Immunosuppressants are fundamental medications for the treatment of RA but carry the risk of inducing HBV reactivation. This inherent contradiction poses challenges throughout the immunosuppressive treatment process in patients with RA. Recently, numerous studies have been conducted on the contradictory therapeutic mechanisms between RA treatment and HBV infection, including aspects of innate immunity, adaptive immunity, and related signalling pathways. In this article, we review the immunological mechanisms underlying the onset of RA and HBV infections, providing a reference for determining appropriate treatment plans to reduce therapeutic contradictions and thereby reduce the risk of HBV reactivation in patients with RA combined with HBV infection.

According to study, anoikis-related genes (ARGs) have been demonstrated to play a significant impact in cirrhosis, a major disease threatening human health worldwide.

To investigate the relationship between ARGs and cirrhosis development to provide insights into the clinical treatment of cirrhosis.

RNA-sequencing data related to cirrhosis were obtained from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between cirrhotic and normal tissues were intersected with ARGs to derive differentially expressed ARGs (DEARGs). The DEARGs were filtered using the least absolute shrinkage and selection operator, support vector machine recursive feature elimination, and random forest algorithms to identify biomarkers for cirrhosis. These biomarkers were used to create a nomogram for predicting the prognosis of cirrhosis. The proportions of diverse immune cell subsets in cirrhotic vs normal tissues were compared using the CIBERSORT computational method. In addition, the linkage between immune cells and biomarkers was assessed, and a regulatory network of mRNA, miRNA, and transcription factors was constructed relying on the biomarkers.

The comparison of cirrhotic and normal tissue samples led to the identification of 635 DEGs. Subsequent intersection of the DEGs with ARGs produced a set of 26 DEARGs. Subsequently, three DEARGs, namely, ACTG1, STAT1, and CCR7, were identified as biomarkers using three machine-learning algorithms. The proportions of M1 and M2 macrophages, resting CD4 memory T cells, resting mast cells, and plasma cells significantly differed between cirrhotic and normal tissue samples. The proportions of M1 and M2 macrophages, resting CD4 memory T cells, and resting mast cells were significantly correlated with the expression of the three biomarkers. The mRNA-miRNA-TF network showed that ACTG1, CCR7, and STAT1 were regulated by 28, 42, and 35 miRNAs, respectively. Moreover, AR, MAX, EP300, and FOXA1 were found to regulate four miRNAs related to the biomarkers.

This study revealed ACTG1, STAT1, and CCR7 as biomarkers of cirrhosis, providing a reference for developing novel diagnostic and therapeutic strategies for cirrhosis.

Mitochondrial damage has a particular impact on the immune system and tumor microenvironment, which can trigger cell stress, an inflammatory response, and disrupt immune cell function, thus all of which can accelerate the progression of the tumor. Therefore, it is of essence to comprehend how the immune system function and the tumor microenvironment interact with mitochondrial dysfunction for cancer treatment. Preserving the integrity of mitochondria or regulating the function of immune cells, such as macrophages, may enhance the efficacy of cancer therapy. Future research should concentrate on the interactions among mitochondria, the immune system, and the tumor microenvironment to identify new therapeutic strategies.

Hepatitis B, a global health concern caused by the hepatitis B virus (HBV), infects nearly 2 billion individuals worldwide, as reported by the World Health Organization (WHO). HBV, a hepatotropic DNA virus, predominantly targets and replicates within hepatocytes. Those carrying the virus are at increased risk of liver cirrhosis and hepatocellular carcinoma, resulting in nearly 900,000 fatalities annually. The HBV X protein (HBx), encoded by the virus's open reading frame x, plays a key role in its virulence. This protein is integral to viral replication, immune modulation, and liver cancer progression. Despite its significance, the precise molecular mechanisms underlying HBx remain elusive. This review investigates the HBx protein's roles in HBV replication, interferon signaling regulation, and hepatocellular carcinoma progression. By understanding the complex interactions between the virus and its host mediated by HBx, we aim to establish a solid foundation for future research and the development of HBx-targeted therapeutics.

To investigate the effect of IFN-α-2b in preventing postoperative arthrofibrosis in rats, its antiproliferation effect on fibroblasts in vitro, and its molecular mechanism.

The rat model of arthrofibrosis was established and treated with different concentrations of drugs. Knee specimens were collected for histological and immunohistochemical staining to observe the effect of IFN-α-2b on arthrofibrosis in rats. The biological information was further mined according to the database data, and the possible regulatory mechanism of IFN-α-2b on fibroblasts was analyzed. The inhibitory effect of IFN-α-2b on fibroblast proliferation and migration in vitro was detected by cell counting kit-8 (CCK-8), immunofluorescence analysis, cell cycle test, EdU assay, wound healing test, and Transwell method, and the analysis results were verified by Western blotting method.

The test results of rat knee joint specimens showed that IFN-α-2b significantly inhibited the degree of fibrosis after knee joint surgery, the number of fibroblasts in the operation area was less than that of the control group, and the expression of collagen and proliferation-related proteins decreased. In vitro experimental results show that IFN-α-2b can inhibit the proliferation and migration of fibroblasts. According to the results of database analysis, it is suggested that the STAT1/P21 pathway may be involved, and it has been verified and confirmed by Western blotting and other related methods.

IFN-α-2b can reduce surgery-induced arthrofibrosis by inhibiting fibroblast proliferation and migration, which may be related to the regulation of STAT1/p21 signaling pathway.

Natural killer (NK) cells are key players in the immune system, however, the exact mechanism of NK cell dysfunction during HBV infection remains poorly defined.

Hepatitis B envelope antigen-negative (HBeAg-, n = 19) chronic hepatitis B infection (CHB) patients, HBeAg-positive (HBeAg+, n = 20) CHB patients, HBV-related hepatocellular carcinoma (HBV-HCC, n = 12) patients and healthy blood donors (HD, n = 20), were enrolled in our study. The phenotype and function of the corresponding NK cells of these subjects were then determined. NK cells were cocultured with HBV to assess whether HBV influences the activation of STAT1. Receptors, proliferation, apoptosis rate, and cytotoxicity of NK-92 cells were detected after STAT1 overexpression and knockdown. The relationship between STAT1 and NKG2D promoter was determined by luciferase assay.

The levels of NKG2D and STAT1 were the lowest in the HBV-HCC group compared with the HD group, followed by the HBeAg+ group and then the HBeAg- group, respectively. Interestingly, STAT1 levels were positively correlated with NKG2D expression and HBeAg status. Furthermore, STAT1 directly bound to the NKG2D promoter to regulate the transcription and expression of NKG2D. Finally, the results also suggested that knockdown of STAT1 can inhibit proliferation, increase apoptosis rate of NK-92 cells and impair cytotoxicity of NK-92 cells.

STAT1 is correlated with NK cell dysfunction by downregulating NKG2D transcription in HBV-infected patients. Our findings demonstrate that STAT1 is an important and positive regulator of NK cells, which could provide a potential immunotherapy target for CHB.