Cystic Fibrosis (CF) is a genetic disease that causes chronic and severe lung inflammation and infection associated with high rates of mortality. In CF, disrupted ion exchange in the epithelium results in excessive mucus production and reduced mucociliary clearance, leading to immune system exacerbation and chronic infections with pathogens such as and . Constant immune stimulation leads to altered immune responses including T cell impairment and neutrophil dysfunction. Specifically, CF is considered a Th17-mediated disease, and it has been proposed that both and a subset of neutrophils known as granulocytic myeloid suppressor cells (gMDSCs) play a role in T cell suppression. The exact mechanisms behind these interactions are yet to be determined, but recent works demonstrate a role for arginase-1. It is also believed that drives gMDSC function as a means of immune evasion, leading to chronic infection. Herein, we review the current literature regarding immune suppression in CF by gMDSCs with an emphasis on T cell impairment and the role of in this dynamic interaction.
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http://dx.doi.org/10.3389/fimmu.2021.745326 | DOI Listing |
Arch Biochem Biophys
January 2025
Department of Pain Management, the First Affiliated Hospital of Jinan University, Guangzhou 510630, China. Electronic address:
Yes-associated protein (YAP), a focal point of current biological research, is involved in regulating various life processes. In this report, live-cell fluorescence resonance energy transfer (FRET) imaging was employed to unravel the YAP complexes in MCF-7 cells. Fluorescence imaging of living cells co-expressing CFP (cyan fluorescent protein)-YAP and YFP (yellow fluorescent protein)-LATS1 (large tumor suppressor 1) plasmids revealed that YAP promoted LATS1 oligomerization around mitochondria.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Department of Biochemistry and Molecular Genetics and.
Mutations or homozygous deletions of MHC class II (MHC-II) genes are commonly found in B cell lymphomas that develop in immune-privileged sites and have been associated with patient survival. However, the mechanisms regulating MHC-II expression, particularly through genetic and epigenetic factors, are not yet fully understood. In this study, we identified a key signaling pathway involving the histone H2AK119 deubiquitinase BRCA1 associated protein 1 (BAP1), the interferon regulatory factor interferon regulatory factor 1 (IRF1), and the MHC-II transactivator class II transactivator (CIITA), which directly activates MHC-II gene expression.
View Article and Find Full Text PDFScientifica (Cairo)
January 2025
Department of Food and Nutritional Sciences, Graduate School of Humanities and Sciences, Ochanomizu University, Tokyo 1128610, Japan.
Although glucosamine (GlcN) exhibits antitumor effects, its mechanism of action remains controversial. Additionally, its impact on hepatocellular carcinoma (HCC) is not well understood. This study aimed to investigate the antitumor effects of GlcN and its underlying mechanism in a mouse HCC cell line, Hepa1-6.
View Article and Find Full Text PDFTransl Cancer Res
December 2024
Department of Oncology, Jiangdu People's Hospital Affiliated to Yangzhou University, Yangzhou, China.
Dipeptidase 1 (DPEP1), initially identified as a renal membrane enzyme in mature human kidneys, plays a pivotal role in various cellular processes. It facilitates the exchange of materials and signal transduction across cell membranes, contributing significantly to dipeptide hydrolysis, glucose and lipid metabolism, immune inflammation, and ferroptosis, among other cellular functions. Extensive research has delineated the complex role of DPEP1 in oncogenesis and tumor progression, with its influence being context dependent.
View Article and Find Full Text PDFEpigenomics
January 2025
Department of Biochemistry, Faculty of Science, Ain Shams University, Cairo, Egypt.
Aims: To investigate the biological impact of simultaneous overexpression of lncRNA MEG3 and miR-155, termed a "double hit," on multiple myeloma (MM) cells compared to individual biomarker substitution.
Materials And Methods: Human MM cells were transfected with MEG3-overexpressed plasmids and miR-155 mimics. Cell cytotoxicity, apoptosis, and gene expression were evaluated in transfected cells and clinical samples.
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