Fatty acid β-oxidation enhances immune regulatory function of double-negative T cells through pSTAT4-OX40 signaling pathway.

Background: Double-negative T (DNT) cells (CD3+CD4-CD8-NK1.1-) demonstrate immunoregulatory functions in maintaining hepatic immune homeostasis. This study investigates how energy metabolism impacts DNT cell survival and immunoregulatory functions, exploring potential therapeutic applications for autoimmune hepatitis.

Histological response and hepatic steatosis changes in nonalcoholic fatty liver disease after bariatric surgery.

Background: Distinguishing bariatric surgical effects on reversing nonalcoholic fatty liver disease (NAFLD) remain unclear. To assess discrepancies in histological response and changes in magnetic resonance imaging-proton density fat fraction (MRI-PDFF) after bariatric surgery.

Methods: This prospective multicenter cohort included 138 NAFLD patients who underwent bariatric surgery and were followed up for 1 year.

Bone Marrow Mesenchymal Stem Cells Can Prevent Pancreatic Fibrosis in Mice with Chronic Pancreatitis by Inhibiting the Activation of Pancreatic Stellate Cells.

Background: Chronic pancreatitis (CP) is a progressive fibroinflammatory disorder primarily driven by a complex interplay of environmental and genetic risk factors. Fibrosis, mediated by activated pancreatic stellate cells (PSCs), represents a key pathological feature of CP. Bone marrow mesenchymal stem cells (BMSCs) are known for their anti-fibrotic and anti-inflammatory properties; however, their role in pancreatic fibrosis remains inadequately understood.

Nitrate protects against methotrexate-induced liver injury by activating Wnt/β-catenin Signaling in mice.

Methotrexate (MTX) is a drug used to treat autoimmune diseases and certain cancers. However, its untreatable hepatotoxic effect severely limits its clinical use. Therefore, further studies are required to combat MTX-induced liver injury.

Rapamycin ameliorates intrahepatic inflammation in MASLD by increasing macrophage fatty acid oxidation levels.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a common liver disease and a serious threat to public health. Mammalian target of rapamycin (mTOR) plays an important role in the progression of MASLD and can be a potential therapeutic target. Our data show that rapamycin treatment can alleviate MASLD symptoms, including liver inflammation, steatosis and steatohepatitis, in the WD, CDHFD- or MCD-induced MASLD mouse model, but has no significant effect on hepatic fibrosis.

The intricate interplay between acute pancreatitis and small intestinal bacterial overgrowth: Unraveling the unknown.

Small intestinal bacterial overgrowth (SIBO) refers to the overcolonization of bacteria in the small intestine. Multiple studies have shown a correlation between SIBO and the occurrence and development of various diseases. This review focuses on the relationship between SIBO and acute pancreatitis (AP), summarizing the current research on the interaction and development between SIBO, AP, and gut microbiota translocation.

Fibrinogen and coagulation factor VIII levels as indicators of disease severity in Hyperlipidemic Acute Pancreatitis: A comparison with biliary etiology.

Background And Aims: Research on the variance of coagulation factors in acute pancreatitis (AP) with different etiologies remains limited. This study aims to explore the coagulation profiles in patients with biliary AP (BAP) and hyperlipidemic AP (HLAP), focusing on their role in predicting disease severity.

Methods: A single-center retrospective cohort study was conducted on patients diagnosed with BAP or HLAP at Beijing Chaoyang Hospital from January 2020 to December 2021.

Estrogen deficiency impairs double-negative T cell function and activates NF-κB in postmenopausal osteoporosis.

Postmenopausal osteoporosis (PMOP), which is driven primarily by estrogen deficiency, is characterized by excessive bone resorption and disrupted immune homeostasis. Although immune system contributions to bone loss are well-documented, the roles of specific regulatory subsets, such as double-negative T (DNT) cells (CD3TCRαβCD4CD8NK1.1), remain unclear.

Isolation of Murine Pancreatic Stellate Cells and the Establishment of a New ex-vivo Activation Model.

Background: Pancreatic stellate cells (PSCs) are critical in the development of pancreatic fibrosis. In vitro, cell attachment itself can promote cell activation. Currently, there is a lack of methods for isolating activated PSCs that are unaffected by cell attachment.

Double-negative T cells in combination with ursodeoxycholic acid ameliorates immune-mediated cholangitis in mice.

Background: Primary biliary cholangitis (PBC) is a liver-specific autoimmune disease. Treatment of PBC with ursodeoxycholic acid (UDCA) is not sufficient to prevent disease progression. Our previous study revealed that the number of hepatic double-negative T cells (DNT), which are unique regulatory T cells, was reduced in PBC patients.

CD73 promotes the immunoregulatory functions of hepatic Tregs through enzymatic and nonenzymatic pathways in MASLD development.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading chronic liver disease characterized by chronic inflammation. Regulatory T cells (Tregs) highly express CD73 and play a critical role in modulating the immune response. However, the roles and mechanisms by which CD73 modulates Tregs in MASLD are still unknown.

Effectiveness of Susceptibility-Guided Therapy for Infection: A Retrospective Analysis by Propensity Score Matching.

Purpose: This study evaluates and compares the eradication rates of Helicobacter pylori (H. pylori) achieved through susceptibility-guided therapy (SGT) based on resistance genotyping and empirical therapy (ET).

Patients And Methods: A retrospective study was conducted at Beijing Chaoyang Hospital (2021-2023) on patients with H.

The T-box transcription factor plays an important role in regulating the immunoregulatory function of double-negative T cells.

Double-negative T (DNT) cells are important immunoregulatory cells that play a key role in maintaining immune homeostasis. However, the specific immune molecular mechanisms regulating DNT cell function have yet to be studied in depth. This study revealed that compared with conventional T cells, natural DNT cells and CD4 T cell-converted DNT (cDNT) cells can secrete high levels of IFN-γ.

Genetic evidence for the liver-brain axis: lipid metabolism and neurodegenerative disease risk.

Background: The liver‒brain axis is critical in neurodegenerative diseases (NDs), with lipid metabolism influencing neuroinflammation and microglial function. A systematic investigation of the genetic relationship between lipid metabolism abnormalities and ND, namely, Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS), is lacking. To assess potential causal links between ND and six lipid parameters, two-sample Mendelian randomization (MR) was used.

CD36-mediated uptake of oxidized LDL induces double-negative regulatory T cell ferroptosis in metabolic dysfunction-associated steatotic liver disease.

Background: Metabolic alterations have been shown to instigate liver inflammation in metabolic dysfunction-associated steatotic liver disease (MASLD), but the underlying mechanism is not fully elucidated. During MASLD progression, intrahepatic CD3TCRαβCD4CD8 double negative T regulatory cells (DNT) decrease cell survival and immunosuppressive function, leading to aggravated liver inflammation. In this study, we aim to reveal the underlying mechanisms that cause changes in DNT during MASLD progression.

Purinergic signaling by TCRαβ double-negative T regulatory cells ameliorates liver ischemia-reperfusion injury.

Hepatic ischemia-reperfusion injury (HIRI) is an important cause of liver injury following liver transplantation and major resections, and neutrophils are the key effector cells in HIRI. Double-negative T regulatory cells (DNT) are increasingly recognized as having critical regulatory functions in the immune system. Whether DNT expresses distinct immunoregulatory mechanisms to modulate neutrophils, as in HIRI, remains largely unknown.

IFITM1 aggravates ConA-Induced autoimmune hepatitis by promoting NKT cell activation through increased AMPK-Dependent mitochondrial function.

Although interferon-induced transmembrane 1 (IFITM1) is known for its crucial role in antiviral immunity, its involvement in autoimmune hepatitis (AIH) remains largely unexplored. In this study, we observed that IFITM1 expression is markedly upregulated in a Concanavalin A (ConA)-induced AIH model, with particularly high and markedly elevated expression in natural killer T (NKT) cells. To further understand the role of IFITM1, we examined the responses of IFITM1 mice in a model of ConA-induced liver injury.

ZNF623 contributes to breast carcinoma progress by recruiting CtBP1 to regulate NF-κB pathway.

Background: Breast cancer ranks among the most prevalent tumor types worldwide. Copy number amplification of chromosome 8q24 is frequently detected in breast cancer. ZNF623 is a relatively unexplored gene mapped to 8q24.

Double-negative T cells ameliorate psoriasis by selectively inhibiting IL-17A-producing γδ T cells.

Background: Psoriasis is a chronic immune-mediated skin condition. Although biologic treatments are effective in controlling psoriasis, some patients do not respond or lose response to these therapies. Thus, new strategies for psoriasis treatment are still urgently needed.

The transcription factor T-bet promotes the pathogenesis of nonalcoholic fatty liver disease by upregulating intrahepatic inflammation.

Objective: To investigate the effect of the transcription factor T-bet on the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and the regulation of the intrahepatic immune microenvironment.

Methods: Wild-type and T-bet knockout NASH mouse models were constructed. The effect of T-bet knockout on the pathogenesis of NAFLD was observed by histochemical staining.

Rebalancing liver-infiltrating CCR3 and CD206 monocytes improves diet-induced NAFLD.

Melatonin has been reported to improve nonalcoholic fatty liver disease (NAFLD), and exploring the underlying mechanisms will be beneficial for better treatment of NAFLD. Choline-deficient high-fat diet (CDHFD)- and methionine/choline-deficient diet (MCD)-fed mice with melatonin intervention exhibit significantly decreased liver steatosis, lobular inflammation, and focal liver necrosis. Single-cell RNA sequencing reveals that melatonin selectively inhibits pro-inflammatory CCR3 monocyte-derived macrophages (MoMFs) and upregulates anti-inflammatory CD206 MoMFs in NAFLD mice.

Inhibition of phospholipase D1 ameliorates hepatocyte steatosis and non-alcoholic fatty liver disease.

Background & Aims: Phospholipase D1 (PLD1), a phosphatidylcholine-hydrolysing enzyme, is involved in cellular lipid metabolism. However, its involvement in hepatocyte lipid metabolism and consequently non-alcoholic fatty liver disease (NAFLD) has not been explicitly explored.

Methods: NAFLD was induced in hepatocyte-specific knockout ((H)-KO) and littermate (-Flox) control mice feeding a high-fat diet (HFD) for 20 wk.

Resveratrol improves hepatic ischemia-reperfusion injury by inhibiting neutrophils via the ERK signaling pathway.

Hepatic ischemia-reperfusion injury (HIRI) is the main complication and even mortality in the setting of hepatic surgery or transplantation. Inflammation, especially the neutrophil response, plays important roles during the process of HIRI. In this study, we found that resveratrol preintervention ameliorated IRI-induced hepatic injury and neutrophil inflammatory responses in the liver.