Natural killer (NK) cell cytotoxic function is critical in guarding an organism against viral infections and malignantly transformed cells. Although the Chromium (Cr)-release assay is regarded as the gold standard for assessing NK cell cytolytic activity, this method is associated with a number of technical problems including the use of radioactive reagents and inconsistent assay performance, due to the lack of assay standardisation across laboratories. Here we describe the setup of a flow cytometry (FC) based method for the measurement of NK cell cytotoxicity, suitable for patient testing. The FC protocol was assessed using four normal samples, and reference values for NK activity of the local Hong Kong population were defined by 40 peripheral blood samples from healthy volunteers. For method validation, we tested a total of 13 specimens including nine healthy individuals and four patients with clinical conditions that were expected to have NK cell dysfunction. We directly compared those results between FC and the Cr-release assay and we were able to demonstrate that FC is a clinically valid method for measuring NK cell function in a clinical setting.
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http://dx.doi.org/10.1016/j.pathol.2018.12.417 | DOI Listing |
Mol Pharm
January 2025
State Key Laboratory for Organic Electronics and Information Displays & Jiangsu Key Laboratory for Biosensors, Institute of Advanced Materials (IAM), Nanjing University of Posts & Telecommunications, Nanjing 210023, China.
Natural killer (NK) cell immunotherapy is a significant category in tumor therapy due to its potent tumor-killing and immunomodulatory effects. This research delves into exploring the mechanisms underlying the ability of amoxicillin to boost NK cell cytotoxicity in NK cell immunotherapy. Amoxicillin significantly enhances the cytotoxic activity of NK-92MI cells against MCF-7 cells by triggering the initiation of a cytolytic program in target cell-deficient NK-92MI cells and augmenting the degranulation level of NK-92MI cells in the presence of target cells.
View Article and Find Full Text PDFJ Exp Med
April 2025
Department of Immunology, Harvard Medical School, Boston, MA, USA.
Inflammatory cytokines are fundamental mediators of the organismal response to injury, infection, or other harmful stimuli. To elucidate the early and mostly direct transcriptional signatures of inflammatory cytokines, we profiled all immunologic cell types by RNAseq after systemic exposure to IL1β, IL6, and TNFα. Our results revealed a significant overlap in the responses, with broad divergence between myeloid and lymphoid cells, but with very few cell-type-specific responses.
View Article and Find Full Text PDFExpert Opin Drug Saf
January 2025
Section of Dermatology - Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy.
Introduction: Bruton's tyrosine kinase (BTK) is a cytoplasmic signaling protein expressed across a variety of immune cells, terminally differentiated plasma cells, and natural killer cells. Due to the signal potential and targetable nature of BTK, the use of BTK inhibitors (BTKis) has been proposed for the management of several diseases. Currently, the use of BTKis is under investigations for several dermatological conditions such as pemphigus, systemic lupus erythematosus, hidradenitis suppurativa, atopic dermatitis, and chronic spontaneous urticaria (CSU).
View Article and Find Full Text PDFKiller whales () have been documented to prey on white sharks (), in some cases causing localised shark displacement and triggering ecological cascades. Notably, a series of such predation events have been reported from South Africa over the last decade, with killer whales specifically targeting sharks' liver. However, observations of these interactions are rare, and knowledge of their frequency across the world's oceans remains limited.
View Article and Find Full Text PDFFront Cardiovasc Med
January 2025
Department of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing, China.
Background: Acute myocardial infarction (AMI), a subset of acute coronary syndrome, remains the major cause of mortality worldwide. Mitochondrial dysfunction is critically involved in AMI progression, and mitophagy plays a vital role in eliminating damaged mitochondria. This study aimed to explore mitophagy-related biomarkers and their potential molecular basis in AMI.
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