<scp>TNF</scp>‐α‐dependent lung inflammation upregulates <scp>PD‐L1</scp> in monocyte‐derived macrophages to contribute to lung tumorigenesis

Yang, Wen; Wang, Xiuqing; Meng, Wei; Guo, Wenli; Duan, Chenyang; Cao, Jingjing; Kang, Lifei; Guo, Ningfei; Lin, Qiang; Lv, Ping; Zhang, Rong; Xing, Lingxiao; Zhang, Xianghong; Shen, Haitao

doi:10.1096/fj.202200434rr

Cited by 7 publications

(7 citation statements)

References 55 publications

(160 reference statements)

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“…There is a signi cant overlap between CD68 and CSN6, and these dates showed CSN6 expression in macrophage in model of sepsis. Wen et al showed that suggested TNF-α upregulated CSN6 expression in lung in ammation [20]. These data showed that CSN6 is involved in the progression of sepsis disease or sepsis-induced myocardial injury.…”

Section: Discussionmentioning

confidence: 91%

CSN6 aggravates inflammation and Myocardial injury in macrophage of sepsis model by MIF

Song,

Zhou,

Liu

et al. 2024

Preprint

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Sepsis, one of the leading causes of death in critically ill patients, is characterized by multiple organ dysfunction caused by dysregulated immune response to infection. Hence, we investigated that the effects of CSN6 in sepsis and the underlying mechanism. RAW264.7 cell inducted with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). CSN6 protein expression of macrophage in vitro model of sepsis was increased. We collected 10 sepsis patients and single cell analysis CSN6 expression. CSN6 aggravated inflammation of macrophage in vitro model of sepsis. CSN6 aggravated ferroptosis of macrophage in vitro model of sepsis. CSN6 aggravated mitochondrial damage of macrophage in vitro model of sepsis. CSN6 induced MIF expression of macrophage in vitro model of sepsis. MIF inhibitor reduced the effects of CSN6 on inflammation and ferroptosis of macrophage in vitro model of sepsis. CSN6 protein at 11-ARG, 21-ARG, 31-LEU, 32-ASP linked MIF protein at 280-ASN, 366-SER.In conclusion, CSN6 aggravates inflammation and myocardial injury in macrophage of sepsis by MIF signaling, suggesting that targeting this mechanism of CSN6 may be a feasible strategy to anti-inflammation for sepsis or sepsis-induced myocardial injury.

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Section: Discussionmentioning

confidence: 91%

CSN6 aggravates inflammation and Myocardial injury in macrophage of sepsis model by MIF

Song,

Zhou,

Liu

et al. 2024

Preprint

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“…Chemokine receptor‐like 2 (CCRL2) can bind with chemokine‐like receptor 1 (CMKLR1) and promote the recruitment of CMKLR1‐expressing immune cells, such as monocytes, DC, and NK cells 28 . The protein expression of CMKLR1 in lung tissues was elevated in a rat model of PAH 29,30 . Cd274, also known as programmed cell death‐ligand 1 (PD‐L1), can bind with programmed death protein‐1 (PD‐1) to inhibit lymphocyte activation and proliferation 31 .…”

Section: Resultsmentioning

confidence: 99%

“… 28 The protein expression of CMKLR1 in lung tissues was elevated in a rat model of PAH. 29 , 30 Cd274, also known as programmed cell death‐ligand 1 (PD‐L1), can bind with programmed death protein‐1 (PD‐1) to inhibit lymphocyte activation and proliferation. 31 A previous study has found that PD‐1 and PD‐L1 proteins were overexpressed on both T and B cells in idiopathic PAH patients, which is similar with our findings.…”

Section: Resultsmentioning

confidence: 99%

Identification of monocyte‐associated pathways participated in the pathogenesis of pulmonary arterial hypertension based on omics‐data

Zhong,

Si,

Yang

et al. 2023

Pulm. circ.

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Pulmonary arterial hypertension (PAH) is one kind of chronic and uncurable diseases that can cause heart failure. Immune microenvironment plays a significant role in PAH. The aim of this study was to assess the role of immune cell infiltration in the pathogenesis of PAH. Differentially expressed genes based on microarray data were enriched in several immune‐related pathways. To evaluate the immune cell infiltration, based on the microarray data sets in the GEO database, we used both ssGSEA and the CIBERSORT algorithm. Additionally, single‐cell RNA sequencing (scRNA‐seq) data was used to further explicit the specific role and intercellular communications. Then receiver operating characteristic curves and least absolute shrinkage and selection operator were used to discover and test the potential diagnostic biomarkers for PAH. Both the immune cell infiltration analyses based on the microarray data sets and the cell proportion in scRNA‐seq data exhibited a significant downregulation in the infiltration of monocytes in PAH. Then, the intercellular communications showed that the interaction weighs of most immune cells, including monocytes changed between the control and PAH groups, and the ITGAL‐ITGB2 and ICAM signaling pathways played critical roles in this process. In addition, ITGAM and ICAM2 displayed good diagnosis values in PAH. This study implicated that the change of monocyte was one of the key immunologic features of PAH. Monocyte‐associated ICAM‐1 and ITGAL‐ITGB2 signaling pathways might be involved in the pathogenesis of PAH.

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“…For one thing, TNF- α can inhibit tumors via activating programmed death cascades in targeted cells, with devastating effects on the function of lysosomal enzymes and/or lysosomal membrane integrity. TNF- α signaling can also be used to induce B7-H1 and PD-L1 expression on CD8 + T cells via several pathways, thereby causing immune resistance [ 25 – 27 ]. We found that three different doses of aconite all increased TNF- α levels in the serum of tumor-bearing mice.…”

Section: Discussionmentioning

confidence: 99%

The Immunoregulatory Effect of Aconite Treatment on H22 Tumor‐Bearing Mice via Modulating Adaptive Immunity and Natural Killer‐Related Immunity

Wang

Jia³

et al. 2023

Evidence-Based Complementary and Alternative Medicine

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Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and, in its advanced stages, has a 5-year survival rate of only 3% to 5%. Despite novel mechanisms and treatments being uncovered over the past few years, effective strategies for HCC are currently limited. Previous studies have proven that aconite can suppress tumor growth and progression and prevent the recurrence and metastasis of multiple cancers, but the underlying molecular mechanisms are largely unknown. In this study, different doses of aconite were applied to mice bearing subcutaneous HCC tumors. It was found that aconite had a therapeutic effect on H22 tumor-bearing mice in a dose-dependent manner by reducing tumor volumes and prolonging survival times, which could be attributed to the immunoregulatory effect of aconite. Furthermore, results showed that high-dose administration of aconite could enhance adaptive immunity and natural killer (NK) cell-mediated immunity by regulating the secretion of interferon-γ, upregulating T cells and NK cells, and modulating the expression of the NK cytotoxicity biomarker CD107a and the inhibitory receptor TIGIT. This study revealed a novel mechanism through which aconite exerts antitumor effects, not merely through apoptosis induction pathways, providing more sound evidence that aconite has the potential to be developed into an effective anti-HCC agent.

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TNF‐α‐dependent lung inflammation upregulates PD‐L1 in monocyte‐derived macrophages to contribute to lung tumorigenesis

Cited by 7 publications

References 55 publications

CSN6 aggravates inflammation and Myocardial injury in macrophage of sepsis model by MIF

CSN6 aggravates inflammation and Myocardial injury in macrophage of sepsis model by MIF

Identification of monocyte‐associated pathways participated in the pathogenesis of pulmonary arterial hypertension based on omics‐data

The Immunoregulatory Effect of Aconite Treatment on H22 Tumor‐Bearing Mice via Modulating Adaptive Immunity and Natural Killer‐Related Immunity

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