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TCR transgenic clone selection guided by immune receptor analysis and single-cell RNA expression of polyclonal responders.
Elife
December 2024
Laboratory of Immunoregulation and Mucosal Immunology, VIB Center for Inflammation Research, Ghent, Belgium.
Since the precursor frequency of naive T cells is extremely low, investigating the early steps of antigen-specific T cell activation is challenging. To overcome this detection problem, adoptive transfer of a cohort of T cells purified from T cell receptor (TCR) transgenic donors has been extensively used but is not readily available for emerging pathogens. Constructing TCR transgenic mice from T cell hybridomas is a labor-intensive and sometimes erratic process, since the best clones are selected based on antigen-induced CD69 upregulation or IL-2 production in vitro, and TCR chains are polymerase chain reaction (PCR)-cloned into expression vectors.
View Article and Find Full Text PDFSecondary metabolites of Alternaria alternate appraisal of their SARS-CoV-2 inhibitory and anti-inflammatory potentials.
PLoS One
January 2025
Department of Pharmacognosy, Faculty of Pharmacy, Helwan University, Cairo, Egypt.
This study identifies the secondary metabolites from Alternaria alternate and evaluates their ACE-2: Spike RBD (SARS-CoV-2) inhibitory activity confirmed via immunoblotting in human lung microvascular endothelial cells. In addition, their in vitro anti-inflammatory potential was assessed using a cell-based assay in LPS-treated RAW 264.7 macrophage cells.
View Article and Find Full Text PDFWeak acid and pepsin reflux induce laryngopharyngeal mucosal barrier injury: A rabbit-model-based study.
PLoS One
January 2025
Department of Otorhinolaryngology, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Objective: Using rabbit models, this study simulated the laryngopharynx's response to the synergistic effects of various acidic reflux environments and pepsin to investigate the response mechanism underlying weak acid reflux and pepsin in the mucosal barrier injury of laryngopharyngeal reflux.
Methods: The rabbits were divided into six groups, and the original larynx was recorded for each group. During the study period, rabbits were sprayed with different doses of acid and pepsin solutions and monitored for hypopharyngeal mucosal transient impedance before and after modeling.
Rspo3-mediated metabolic liver zonation regulates systemic glucose metabolism and body mass in mice.
PLoS Biol
January 2025
Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.
The unique architecture of the liver consists of hepatic lobules, dividing the hepatic features of metabolism into 2 distinct zones, namely the pericentral and periportal zones, the spatial characteristics of which are broadly defined as metabolic zonation. R-spondin3 (Rspo3), a bioactive protein promoting the Wnt signaling pathway, regulates metabolic features especially around hepatic central veins. However, the functional impact of hepatic metabolic zonation, regulated by the Rspo3/Wnt signaling pathway, on whole-body metabolism homeostasis remains poorly understood.
View Article and Find Full Text PDFStructure-guided engineering of a mutation-tolerant inhibitor peptide against variable SARS-CoV-2 spikes.
Proc Natl Acad Sci U S A
January 2025
Cellular and Structural Physiology Laboratory, Advanced Research Initiative, Institute of Integrated Research, Institute of Science Tokyo, Bunkyo-ku, Tokyo 113-8510, Japan.
Pathogen mutations present an inevitable and challenging problem for therapeutics and the development of mutation-tolerant anti-infective drugs to strengthen global health and combat evolving pathogens is urgently needed. While spike proteins on viral surfaces are attractive targets for preventing viral entry, they mutate frequently, making it difficult to develop effective therapeutics. Here, we used a structure-guided strategy to engineer an inhibitor peptide against the SARS-CoV-2 spike, called CeSPIACE, with mutation-tolerant and potent binding ability against all variants to enhance affinity for the invariant architecture of the receptor-binding domain (RBD).
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