Sex and age-matched wild-type and TCR transgenic mice were infected with cytomegalovirus (CMV) at 6 months of age and followed for 12 additional months to examine aging of the immune system. It was found that viral infection of C57Bl/6 mice resulted in accelerated aging of the immune system as shown by a loss of CD8(+)28(+) cells and an accumulation of KLRG1(+) T cells. CMV infection of OT-1 transgenic mice had no influence on immune aging of these mice which nonetheless demonstrated an accumulation of CD8(+)28(-) and KLRG1(+) T cells with time. CD4(+) T cells were unaffected in either strain of mice. Thus, immunological aging was found to be due to both cell-intrinsic and cell-extrinsic factors. Persistent viral infections may accelerate immunological aging but consideration must be given to individual variation in the aging process.
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http://dx.doi.org/10.1016/j.imbio.2014.02.008 | DOI Listing |
Cardiovasc Diabetol
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Institute of Physiology, iCBR, Faculty of Medicine, University of Coimbra, Subunit 1, polo 3, Azinhaga de Santa Comba, Celas, 3000-548, Coimbra, Portugal.
Perivascular adipose tissue (PVAT) is a dynamic tissue that affects vascular function and cardiovascular health. The connection between PVAT, the immune system, obesity, and vascular disease is complex and plays a pivotal role in the pathogenesis of vascular diseases such as atherosclerosis, hypertension, and vascular inflammation. In cardiometabolic diseases, PVAT becomes a significant source of proflammatory adipokines, leading to increased infiltration of immune cells, in cardiometabolic diseases, PVAT becomes a significant source of proinflammatory adipokines, leading to increased infiltration of immune cells, promoting vascular smooth muscle cell proliferation and migrationpromoting vascular smooth muscle cell proliferation and migration.
View Article and Find Full Text PDFBMC Complement Med Ther
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Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.
Background: A precise observation is that the cervix's solid tumors possess hypoxic regions where the oxygen concentration drops below 1.5%. Hypoxia negatively impacts the host's immune system and significantly diminishes the effectiveness of several treatments, including radiotherapy and chemotherapy.
View Article and Find Full Text PDFFEMS Microbiol Rev
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Junior Research Group Adaptive Pathogenicity Strategies, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute, Jena, Germany.
Pathogenic microorganisms can infect a variety of niches in the human body. During infection, microbes can only persist if they adapt adequately to the dynamic host environment and the stresses imposed by the immune system. While viruses entirely rely on host cells to replicate, bacteria and fungi use their pathogenicity mechanisms for the acquisition of essential nutrients that lie under host restriction.
View Article and Find Full Text PDFTrends Biotechnol
December 2024
Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA; Department of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA. Electronic address:
Immune system functions play crucial roles in both health and disease, and these functions are regulated by their metabolic programming. The field of immune engineering has emerged to develop therapeutic strategies, including polymeric nanoparticles (NPs), that can direct immune cell phenotype and function by directing immunometabolic changes. Precise control of bioenergetic processes may offer the opportunity to prevent undesired immune activity and improve disease-specific outcomes.
View Article and Find Full Text PDFTrends Mol Med
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Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, PA, USA. Electronic address:
Genetic and epigenetic defects of the p53 system have previously been associated with resistance to CDK4/6 inhibitors in women with HR breast cancer. Recent data from Kudo et al. demonstrate that CDK2-targeting agents may offer an effective strategy to circumvent such resistance by enforcing cellular senescence downstream of RBL2 dephosphorylation.
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