CXCR6 deficiency ameliorates ischemia-reperfusion injury by reducing the recruitment and cytokine production of hepatic NKT cells in a mouse model of non-alcoholic fatty liver disease

Zhu, Huanbing; Zhang, Qi; Chen, Guihua

doi:10.1016/j.intimp.2019.04.021

Cited by 23 publications

(29 citation statements)

References 44 publications

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“…Meanwhile, the inhibition of ACAT1 strengthens the tumor-limiting activities of CD19-CAR-T cells by elevating the ratio of effector-to-target cells even under low infection rates and could rescue CD8 + T cell inhibition in chemo-immunotherapy [ 60 , 61 ]. Moreover, natural killer T (NKT) cells, a cluster of CD1d restricted T cells that simultaneously possess the characteristics of adaptive and innate immune cells, mostly recognize lipid antigens and exert multiple immunoregulatory effects [ 62 ]. Thus, lipids can regulate the cytotoxicity of NKT cells.…”

Section: Anti-tumor Effects Of Lipids In Tumor Immune Responsementioning

confidence: 99%

Contradictory roles of lipid metabolism in immune response within the tumor microenvironment

Lei

et al. 2021

J Hematol Oncol

117

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Complex interactions between the immune system and tumor cells exist throughout the initiation and development of cancer. Although the immune system eliminates malignantly transformed cells in the early stage, surviving tumor cells evade host immune defense through various methods and even reprogram the anti-tumor immune response to a pro-tumor phenotype to obtain unlimited growth and metastasis. The high proliferation rate of tumor cells increases the demand for local nutrients and oxygen. Poorly organized vessels can barely satisfy this requirement, which results in an acidic, hypoxic, and glucose-deficient tumor microenvironment. As a result, lipids in the tumor microenvironment are activated and utilized as a primary source of energy and critical regulators in both tumor cells and related immune cells. However, the exact role of lipid metabolism reprogramming in tumor immune response remains unclear. A comprehensive understanding of lipid metabolism dysfunction in the tumor microenvironment and its dual effects on the immune response is critical for mapping the detailed landscape of tumor immunology and developing specific treatments for cancer patients. In this review, we have focused on the dysregulation of lipid metabolism in the tumor microenvironment and have discussed its contradictory roles in the tumor immune response. In addition, we have summarized the current therapeutic strategies targeting lipid metabolism in tumor immunotherapy. This review provides a comprehensive summary of lipid metabolism in the tumor immune response.

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Section: Anti-tumor Effects Of Lipids In Tumor Immune Responsementioning

confidence: 99%

Contradictory roles of lipid metabolism in immune response within the tumor microenvironment

Lei

et al. 2021

J Hematol Oncol

117

View full text Add to dashboard Cite

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“…NKT cells are CD1d restricted and recognize lipid antigens. 33 Therefore, altered tumor lipid metabolism is supposed to affect the antigen recognition function of NKT cells. Lipid metabolism can also impair the antigen-presenting ability of DC, thereby facilitating immunosuppression.…”

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confidence: 99%

Development and Validation of a Metabolic Gene-Based Prognostic Signature for Hepatocellular Carcinoma

Weng¹,

Zhou²,

Zhou³

et al. 2021

JHC

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Background: Hepatocellular carcinoma (HCC) is a malignant tumor with great variation in prognosis among individuals. Changes in metabolism influence disease progression and clinical outcomes. The objective of this study was to determine the overall survival (OS) risk of HCC patients from a metabolic perspective. Patients and Methods: The model was constructed using the least absolute shrinkage and selection operator (LASSO) COX regression based on The Cancer Genome Atlas (TCGA, n=342) dataset. The International Cancer Genome Consortium (ICGC, n=232), GSE14520 (n=242) datasets, and a clinical cohort (n=64) were then used to assess the prognostic value of the signature. Results: A 10 metabolic gene-based signature was constructed and verified as a robust and independent prognostic classifier in public and real-world validation cohorts. Meanwhile, the signature enabled the identification of HCC molecular subtypes, yielding an AUC value of 0.678 [95% CI: 0.592-0.763]. Besides, the signature was associated with metabolic processes like glycolysis, supported by a clear correlation between the risk score and expression of rate-limiting enzymes. Furthermore, high-risk tumor was likely to have a high tumor infiltration status of immunosuppressive cells, as well as elevated expression of some immune checkpoint molecules. For final clinical translation, a nomogram integrating the signature and tumor stage was established, and showed improved predictive accuracy of 3and 5-year OS and brought more net benefit to patients. Conclusion:We developed a prognostic signature based on 10 metabolic genes, which has proven to be an independent and reliable prognostic predictor for HCC and reflects the metabolic and immune characteristics of tumors.

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“…In addition, the frequency of iNKT cells was increased in peripheral blood mononuclear cells (PBMCs) from NASH patients compared to that in healthy controls. The axis of CXCR6/CXCL16 plays an essential role in the recruitment of NKT cells in fatty liver, liver fibrosis, and liver cancer [ 60 , 61 ]. Gut microbiota such as Clostridium spp.…”

Section: Intrahepatic Immunity In Nafld and Nash In Diet-induced Murine Models And Human Patientsmentioning

confidence: 99%

Diet and Gut Microbiota Interaction-Derived Metabolites and Intrahepatic Immune Response in NAFLD Development and Treatment

Yang

Khoukaz

et al. 2021

Biomedicines

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Nonalcoholic fatty liver disease (NAFLD) with pathogenesis ranging from nonalcoholic fatty liver (NAFL) to the advanced form of nonalcoholic steatohepatitis (NASH) affects about 25% of the global population. NAFLD is a chronic liver disease associated with obesity, type 2 diabetes, and metabolic syndrome, which is the most increasing factor that causes hepatocellular carcinoma (HCC). Although advanced progress has been made in exploring the pathogenesis of NAFLD and penitential therapeutic targets, no therapeutic agent has been approved by Food and Drug Administration (FDA) in the United States. Gut microbiota-derived components and metabolites play pivotal roles in shaping intrahepatic immunity during the progression of NAFLD or NASH. With the advance of techniques, such as single-cell RNA sequencing (scRNA-seq), each subtype of immune cells in the liver has been studied to explore their roles in the pathogenesis of NAFLD. In addition, new molecules involved in gut microbiota-mediated effects on NAFLD are found. Based on these findings, we first summarized the interaction of diet-gut microbiota-derived metabolites and activation of intrahepatic immunity during NAFLD development and progression. Treatment options by targeting gut microbiota and important molecular signaling pathways are then discussed. Finally, undergoing clinical trials are selected to present the potential application of treatments against NAFLD or NASH.

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CXCR6 deficiency ameliorates ischemia-reperfusion injury by reducing the recruitment and cytokine production of hepatic NKT cells in a mouse model of non-alcoholic fatty liver disease

Cited by 23 publications

References 44 publications

Contradictory roles of lipid metabolism in immune response within the tumor microenvironment

Contradictory roles of lipid metabolism in immune response within the tumor microenvironment

Development and Validation of a Metabolic Gene-Based Prognostic Signature for Hepatocellular Carcinoma

Diet and Gut Microbiota Interaction-Derived Metabolites and Intrahepatic Immune Response in NAFLD Development and Treatment

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