Phagocytosis is the cellular defense mechanism used to eliminate antigens derived from dysregulated or damaged cells, and microbial pathogens. Phagocytosis is therefore a pillar of innate immunity, whereby foreign particles are engulfed and degraded in lysolitic vesicles. In hexacorallians, phagocytic mechanisms are poorly understood, though putative anthozoan phagocytic cells (amoebocytes) have been identified histologically. We identify and characterize phagocytes from the coral and the sea anemone . Using fluorescence-activated cell sorting and microscopy, we show that distinct populations of phagocytic cells engulf bacteria, fungal antigens, and beads. In addition to pathogenic antigens, we show that phagocytic cells engulf self, damaged cells. We show that target antigens localize to low pH phagolysosomes, and that degradation is occurring within them. Inhibiting actin filament rearrangement interferes with efficient particle phagocytosis but does not affect small molecule pinocytosis. We also demonstrate that cellular markers for lysolitic vesicles and reactive oxygen species (ROS) correlate with hexacorallian phagocytes. These results establish a foundation for improving our understanding of hexacorallian immune cell biology.
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http://dx.doi.org/10.3389/fimmu.2021.662803 | DOI Listing |
J Occup Health
January 2025
Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Objectives: Natural fibrous mineral, asbestos, has been useful in industry for many centuries. In the 1960's, epidemiology had recognized the association between asbestos exposure and mesothelioma and the IARC designated all kinds of asbestos as Group 1 in 1987. However, various scientific enigmas remained regarding the molecular mechanisms of asbestos-induced mesothelial carcinogenesis.
View Article and Find Full Text PDFSci Rep
January 2025
General Surgery Department, Jiangsu University Affiliated People's Hospital, Zhenjiang, 212000, China.
Crohn's disease (CD) is a chronic inflammatory bowel disease with an unknown etiology. Ubiquitination plays a significant role in the pathogenesis of CD. This study aimed to explore the functional roles of ubiquitination-related genes in CD.
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January 2025
Department of Dermatology, Dermatology Hospital of Zhejiang Province, Huzhou, 313299, China.
Although an ongoing understanding of psoriasis vulgaris (PV) pathogenesis, little is known about the proteomic differences between moderate and severe psoriasis. In this cross-sectional study, we evaluated the proteomic differences between moderate and severe psoriasis using data-independent acquisition mass spectrometry (DIA-MS). 173 differentially expressed proteins (DEPs) were significantly differentially expressed between the two groups.
View Article and Find Full Text PDFNat Commun
January 2025
MRC Laboratory of Medical Sciences, London, UK.
Gene enhancers often form long-range contacts with promoters, but it remains unclear if the activity of enhancers and their chromosomal contacts are mediated by the same DNA sequences and recruited factors. Here, we study the effects of expression quantitative trait loci (eQTLs) on enhancer activity and promoter contacts in primary monocytes isolated from 34 male individuals. Using eQTL-Capture Hi-C and a Bayesian approach considering both intra- and inter-individual variation, we initially detect 19 eQTLs associated with enhancer-eGene promoter contacts, most of which also associate with enhancer accessibility and activity.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Division of Infection, Immunity and Respiratory Medicine, The University of Manchester, Manchester, UK
Background: Programmed cell death 1 (PD-1) signaling blockade by immune checkpoint inhibitors (ICI) effectively restores immune surveillance to treat melanoma. However, chronic interferon-gamma (IFNγ)-induced immune homeostatic responses in melanoma cells contribute to immune evasion and acquired resistance to ICI. Poly ADP ribosyl polymerase 14 (PARP14), an IFNγ-responsive gene product, partially mediates IFNγ-driven resistance.
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