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| http://dx.doi.org/10.1161/ATVBAHA.122.317830 | DOI Listing |
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Ubiquitin-Conjugating Enzyme Ubc13 in Macrophages Suppresses Lung Tumor Progression Through Inhibiting PD-L1 Expression.
Eur J Immunol
December 2024
Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Tumor cell-intrinsic ubiquitin-conjugating enzyme Ubc13 promotes tumorigenesis, yet how Ubc13 in immune cell compartments regulates tumor progression remains elusive. Here, we show that myeloid-specific deletion of Ubc13 (Ubc13Lyz2) leads to accelerated transplanted lung tumor growth in mice. Compared with their littermate controls, tumor-bearing Ubc13Lyz2 mice had lower proliferation and effector function of CD8 T lymphocytes, accompanied by increased infiltration of myeloid-derived suppressor cells within the tumor microenvironment.
View Article and Find Full Text PDFTime-of-day control of mitochondria regulates NLRP3 inflammasome activation in macrophages.
FASEB J
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Curtis Clock Laboratory, School of Pharmacy and Biomolecular Sciences (PBS), Royal College of Surgeons in Ireland (RCSI), Dublin, Ireland.
Macrophages are innate immune cells that orchestrate the process of inflammation, which varies across time of day. This ensures appropriate biological timing of the immune response with the external environment. The NLRP3 inflammasome mediates IL-1-family cytokine release via pyroptosis.
View Article and Find Full Text PDFSmad4 Deficiency in S100A4 Macrophages Enhances Colitis-associated Tumorigenesis by Promoting Macrophage Lipid Metabolism Augmented M2 Polarization.
Int J Biol Sci
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The College of Life Science and Bioengineering, Beijing Jiaotong University, Beijing, P.R. China.
S100A4 is primarily expressed in intestinal macrophages, and promotes colonic inflammation and colitis-associated colon tumorigenesis. Smad4 is also expressed in the colon; however, it inhibits colitis-associated cancer (CAC) development. The specific role of Smad4 in S100A4 cells in CAC remains unknown.
View Article and Find Full Text PDFMacrophage Dvl2 deficiency promotes NOD1-Driven pyroptosis and exacerbates inflammatory liver injury.
Redox Biol
December 2024
The Dumont-UCLA Transplant Center, Division of Liver and Pancreas Transplantation, Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Electronic address:
Dishevelled 2 (Dvl2) is a key mediator of the Wingless/Wnt signaling pathway that regulates cell proliferation, migration, and immune function. However, little is known about the role of macrophage Dvl2 in modulating NOD1-mediated pyroptosis and hepatocyte death in oxidative stress-induced inflammatory liver injury. In a mouse model of oxidative stress-induced liver inflammation, mice with myeloid-specific Dvl2 knockout (Dvl2) displayed exacerbated ischemia/reperfusion (IR) stress-induced hepatocellular damage with increased serum ALT levels, oxidative stress, and proinflammatory mediators.
View Article and Find Full Text PDFNeutrophil CRACR2A Promotes Neutrophil Recruitment in Sterile Inflammation and Ischemic Stroke.
Circulation
November 2024
Division of Hematology, Department of Medicine, Washington University School of Medicine, St Louis, MO. (J.L., B.B., A.S., V.K., J.C.).
Background: Ca release-activated Ca channel regulator 2A (CRACR2A) has been linked to immunodeficiency attributable to T-cell dysfunction in humans. We discovered that neutrophil CRACR2A promotes neutrophil adhesive and migratory functions by facilitating Ca mobilization and β2 integrin activation.
Methods: Myeloid-specific cracr2a conditional knockout mice and intravital microscopy were used to investigate the physiologic role of neutrophil cracr2a in neutrophil recruitment in vascular inflammation.
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