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| http://dx.doi.org/10.3324/haematol.2023.284050 | DOI Listing |
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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Ronald M. Loeb Center for Alzheimer's Disease, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: While compelling evidence highlights the importance of myeloid cells in the etiology of Alzheimer's Disease (AD), the relevance of immunometabolism still requires further exploration. Our analysis integrating AD genetics and myeloid cell genomics shows that lower levels of LACTB expression in myeloid cells is protective against AD, a finding supported by proteomics studies. As a mitochondrial active-site serine protein, LACTB has implications for mitochondrial morphology and bioenergetics.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Washington University in St. Louis, School of Medicine, St. Louis, MO, USA.
Article Synopsis
- Therapeutics targeting human genetics are more successful in clinical trials compared to standard FDA approved drugs.
- In 2012, the Alzheimer's Disease Sequencing Project (ADSP) was initiated to enhance understanding of Alzheimer's disease and speed up treatment development through large-scale genetic analysis.
- The project identified over a hundred genetic loci linked to Alzheimer's and highlighted the role of immune cells like microglia in disease risk, leading to potential immunotherapies that target specific related pathways.
Innate immune cells link dietary cues to normal and abnormal metabolic regulation.
Nat Immunol
January 2025
Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
A slew of common metabolic disorders, including type 2 diabetes, metabolic dysfunction-associated steatotic liver disease and steatohepatitis, are exponentially increasing in our sedentary and overfed society. While macronutrients directly impact metabolism and bioenergetics, new evidence implicates immune cells as critical sensors of nutritional cues and important regulators of metabolic homeostasis. A deeper interrogation of the intricate and multipartite interactions between dietary components, immune cells and metabolically active tissues is needed for a better understanding of metabolic regulation and development of new treatments for common metabolic diseases.
View Article and Find Full Text PDFSIRT7 Promotes Alcohol Associated Liver Injury via Modulating Myeloid Cell CCL2 Secretion through NF-κB Signaling Pathway.
Am J Pathol
December 2024
The Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, The Key Laboratory of Model Animals and Stem Cell Biology of Hunan Province, Engineering Research Center of Reproduction and Translational Medicine of Hunan Province, and Institute of Interdisciplinary Studies, Hunan Normal University School of Pharmaceutical Science, Changsha, Hunan, 410013 China. Electronic address:
Article Synopsis
- The progression of Alcohol-associated liver disease (ALD) involves increased gut permeability due to ethanol, leading to bacterial products entering the bloodstream and causing liver inflammation and damage.
- The study used mice without the SIRT7 gene in myeloid cells, finding that this knockout reduced liver injury and inflammation caused by alcohol while minimally impacting lipid metabolism.
- Identification of CCL2 as a key target affected by SIRT7 highlights how its knockout hinders macrophage CCL2 secretion and monocyte recruitment, suggesting that targeting SIRT7 could provide new treatment strategies for ALD.
Lung cancer-intrinsic SOX2 expression mediates resistance to checkpoint blockade therapy by inducing Treg cell-dependent CD8+ T-cell exclusion.
Cancer Immunol Res
January 2025
Massachusetts Institute of Technology, Cambridge, MA, United States.
Tumor cell-intrinsic signaling pathways can drastically affect the tumor immune microenvironment, promoting tumor progression and resistance to immunotherapy by excluding immune-cell populations from the tumor. Several tumor cell-intrinsic pathways have been reported to modulate myeloid-cell and T-cell infiltration creating "cold" tumors. However, clinical evidence suggests that excluding cytotoxic T cells from the tumor core also mediates immune evasion.
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