Targeting Deltex E3 Ubiquitin Ligase 2 Inhibits Tumor‐associated Neutrophils and Sensitizes Hepatocellular Carcinoma Cells to Immunotherapy DOI Creative Commons
Xiaoling Wu, Jiafeng Chen, Yiran Chen

et al.

Advanced Science, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 29, 2024

Abstract Several E3 ligases have been found to affect the immune microenvironment of hepatocellular carcinoma (HCC) and lead resistance immunotherapy. In this study, genes are screened based on The Cancer Genome Atlas (TCGA) dataset. Through cytometry by time flight (CyTOF), flow cytometry, further experiments, Deltex ubiquitin ligase 2 (DTX2) in HCC cells is identified promote infiltration polarization tumor‐associated neutrophils (TANs) with a protumor phenotype, thus attenuating cytotoxicity CD8+ T partially through C‐X‐C motif chemokine (CXCL2) 6 (CXCL6). Mechanistically, DTX2 can interact histone H2B its monoubiquitination at lysine120 (H2BK120ub1), thereby increasing CXCL2 CXCL6 transcription epigenetic regulation. Different tumor models vivo demonstrated that inhibitor treatment inhibited growth sensitized therapeutic effects programmed cell death protein 1 (PD‐1) antibody. summary, study identifies as potential target for

Language: Английский

The temporal progression of lung immune remodeling during breast cancer metastasis DOI
Christopher S. McGinnis, Zhuang Miao, Daphne Superville

et al.

Cancer Cell, Journal Year: 2024, Volume and Issue: 42(6), P. 1018 - 1031.e6

Published: May 30, 2024

Language: Английский

Citations

15
Kawasaki disease: contemporary perspectives DOI

Megan Day‐Lewis,

Mary Beth F. Son, Mindy S. Lo

et al.

The Lancet Child & Adolescent Health, Journal Year: 2024, Volume and Issue: 8(10), P. 781 - 792

Published: Sept. 17, 2024

Language: Английский

Citations

6
Risk factors for predicting medium-giant coronary artery aneurysms in Kawasaki disease DOI
Li Zhao, Jiangping Wu, Xiaoliang Liu

et al.

Immunologic Research, Journal Year: 2025, Volume and Issue: 73(1)

Published: Feb. 17, 2025

Language: Английский

Citations

0
S100A12 triggers NETosis to aggravate myocardial infarction injury via the Annexin A5-calcium axis DOI Creative Commons
Xi Zhang,

Haixu Song,

Dan Liu

et al.

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: Feb. 18, 2025

Neutrophil extracellular traps (NETs) play a critical role in acute myocardial infarction (AMI) and the externalization of S100 family members. Here, we show effects S100A12 on NETs formation injury following AMI. expression increases rapidly neutrophils peaks day 1 after AMI, promoting production exacerbating injury. DNase I, an inhibitor NETs, reduces apoptosis cardiomyocytes induced by S100A12. Mechanistically, interaction Annexin A5 (ANXA5) enhances calcium influx promotes formation. Blockage ANXA5 effectively attenuates heart function impairment Finally, that plasma levels correlate with dsDNA concentration, this correlation is associated increased risk all-cause mortality during 1-year follow-up AMI patients. These findings, derived from male mice, reveal S100A12-ANXA5-calcium axis as potential therapeutic target biomarker for contribute to damage (AMI). authors worsens injury, whereas blocking its damage, suggesting new

Language: Английский

Citations

0
Integrated single-cell and spatial transcriptomic profiling reveals that CD177+ Tregs enhance immunosuppression through apoptosis and resistance to immunotherapy in hepatocellular carcinoma DOI
Yuan Liang,

Lei Qiao,

Qufei Qian

et al.

Oncogene, Journal Year: 2025, Volume and Issue: unknown

Published: March 7, 2025

Language: Английский

Citations

0
Aberrant expansion of CD177+ neutrophils promotes endothelial dysfunction in systemic lupus erythematosus via neutrophil extracellular traps DOI

H. Xu,

Minghua Zhan,

Ziyan Wu

et al.

Journal of Autoimmunity, Journal Year: 2025, Volume and Issue: 152, P. 103399 - 103399

Published: March 1, 2025

Language: Английский

Citations

0
Long-term cardiovascular inflammation and fibrosis in a murine model of vasculitis induced by Lactobacillus casei cell wall extract DOI Creative Commons
Ana Paula Lombardi Pereira, Emily Aubuchon,

Debbie Moreira

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: June 25, 2024

Kawasaki disease (KD), an acute febrile illness and systemic vasculitis, is the leading cause of acquired heart in children industrialized countries. KD leads to development coronary artery aneurysms (CAA) affected children, which may persist for months even years after phase disease. There unmet need characterize immune pathological mechanisms long-term complications KD. We examined cardiovascular Lactobacillus casei cell wall extract (LCWE) mouse model KD-like vasculitis over 4 months. The immune, pathological, functional changes occurring lesions were characterized by histological examination, flow cytometric analysis, immunofluorescent staining tissues, transthoracic echocardiogram. CAA abdominal aorta dilations detected up 16 weeks following LCWE injection initiation vasculitis. observed alterations composition circulating profiles, such as increased monocyte frequencies higher counts neutrophils. determined a positive correlation between neutrophil inflammatory severity early injection. LCWE-induced was associated with myocarditis myocardial dysfunction, diminished ejection fraction left ventricular remodeling, worsened time. extensive fibrosis within inflamed cardiac tissue later stages. Our findings indicate that are reliable predictor inflammation LCWE-injected mice. Furthermore, stemming from infiltrations aortic root arteries, long periods still

Language: Английский

Citations

3
Hypovitaminosis D and Leukocytosis to Predict Cardiovascular Abnormalities in Children with Kawasaki Disease: Insights from a Single-Center Retrospective Observational Cohort Study DOI Creative Commons
Donato Rigante, Gabriella De Rosa, Angelica Bibiana Delogu

et al.

Diagnostics, Journal Year: 2024, Volume and Issue: 14(12), P. 1228 - 1228

Published: June 12, 2024

An aberrant immune response involving yet unidentified environmental and genetic factors plays a crucial role in triggering Kawasaki disease (KD).

Language: Английский

Citations

1
Exploration of common genomic signatures of Systemic juvenile rheumatoid arthritis and Kawasaki disease DOI Creative Commons

Shiling Zhong,

Ling Wu,

Yunyan Li

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: May 6, 2024

Abstract To investigate the common genetic patterns and possible molecular processes involved in systemic juvenile idiopathic arthritis (SJIA) Kawasaki disease (KD). The methodology retrieval analysis of microarray data for SJIA KD from Gene Expression Omnibus (GEO) database. researchers employed ExpressAnalystR software to ascertain differentially expressed genes (DEGs) that were shared, subsequently identified associated with extracellular proteins within this set. Transcription factors (TFs) their corresponding target single-domain encoding (SDEGs) acquired by a comparative databases such as HumanTFDB hTFtarget. Subsequently, gene sets had been previously underwent functional enrichment using metascape program. Ultimately, immune infiltration was conducted CIBERSORT. study revealed total 204 up-regulated 35 down-regulated SDEGs. Through construction network targeting transcription (TFs), 4 specific TFs (EGR1, BCL6, FOS, NFE2) further screened. Functional findings indicate both adaptive innate systems play significant roles development Signaling pathways, NF-kB, are crucial pathogenesis these conditions, along biological like tumor necrosis factor (TNF) functions neutrophil degranulation. our investigation provided comprehensive evidence regarding intricate adaptable nature system abnormalities KD. same pathogenic mechanism may involve actions TNF, degranulation, NF-kB pathway. Furthermore, it is imperative carry out more regulatory EGR1, NFE2 network.

Language: Английский

Citations

0
Neutrophil Heterogeneity Is Modified during Acute Lung Inflammation in Apoa1−/− Mice DOI
Xianglan Yao, Neelam Redekar, Karen J. Keeran

et al.

The Journal of Immunology, Journal Year: 2024, Volume and Issue: unknown

Published: June 24, 2024

Abstract Neutrophils play important roles in inflammatory airway diseases. In this study, we assessed whether apolipoprotein A-I modifies neutrophil heterogeneity as part of the mechanism by which it attenuates acute inflammation. Neutrophilic inflammation was induced daily intranasal administration LPS plus house dust mite (LPS+HDM) to Apoa1−/− and Apoa1+/+ mice for 3 d. Single-cell RNA sequencing performed on cells recovered from bronchoalveolar lavage fluid day 4. Unsupervised profiling identified 10 clusters neutrophils mice. LPS+HDM-challenged had an increased proportion Neu4 cluster that expressed S100a8, S100a9, Mmp8 high maturation, aggregation, TLR4 binding scores. There also increase Neu6 immature neutrophils, whereas expressing IFN-stimulated genes were decreased. An unsupervised trajectory analysis showed represented a distinct lineage recruited airspace macrophages, associated with reciprocal reduction resident macrophages. Increased expression common set proinflammatory genes, Lcn2, present all macrophages These findings show have increases specific macrophage lung during mediated LPS+HDM, well enhanced genes. This suggests modifications contribute

Language: Английский

Citations

0