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http://dx.doi.org/10.1007/s10875-022-01321-6 | DOI Listing |
Nat Commun
December 2024
Department of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA.
The development of pancreatic cancer requires both, acquisition of an oncogenic mutation in KRAS as well as an inflammatory insult. However, the physiological causes for pancreatic inflammation are less defined. We show here that oncogenic KRas-expressing pre-neoplastic lesion cells upregulate coxsackievirus (CVB) and adenovirus receptor (CAR).
View Article and Find Full Text PDFRev Med Virol
November 2024
Laboratoire de Virologie URL3610, Univ. Lille et CHU Lille, Lille, France.
Enteroviruses (EV) initiate replication by binding to their cellular receptors, leading to the uncoating and release of the viral genome into the cytosol of the host cell. Neutralising antibodies (NAbs) binding to epitopes on enteroviral capsid proteins can inhibit this infectious process through several mechanisms of neutralisation in vitro. Fc-mediated antibody effector functions such as antibody-dependent cell-mediated cytotoxicity and antibody-dependent cellular phagocytosis have also been described for some EV.
View Article and Find Full Text PDFDiabetes
October 2024
Department of Genetics and Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Persistent enterovirus B infection has been proposed as an important contributor to the etiology of type 1 diabetes. We leveraged extensive bulk RNA-sequencing (RNA-seq) data from α-, β-, and exocrine cells, as well as islet single-cell RNA-seq data from the Human Pancreas Analysis Program (HPAP), to evaluate the presence of enterovirus B sequences in the pancreas of patients with type 1 diabetes and prediabetes (no diabetes but positive for autoantibodies). We examined all available HPAP data for either assay type, including donors without diabetes and with type 1 and type 2 diabetes.
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