Dendritic cells (DCs) are key antigen-presenting cells (APCs) that act as central modulators of cellular immune responses. Genetic modification of DCs has considerable therapeutic potential in the treatment of a wide spectrum of diseases, including cancer and persistent viral infection. In this report, we show that pre-treatment of DCs with a recombinant adenovirus encoding the major adenovirus receptor, Coxsackie B and adenovirus receptor (CAR), significantly increased the uptake of recombinant adenoviruses (Ads) by primary immature monocyte-derived DCs. This could be correlated with CAR mRNA and surface protein expression. Transduction of DCs by recombinant adenoviruses did not significantly alter cellular viability. Therefore, we propose that pre-treatment of DCs with Ad5-CAR is one strategy to increase the susceptibility of DCs to transduction by recombinant Ads.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s0022-1759(01)00510-5 | DOI Listing |
Viruses
November 2024
Department of Veterinary Pathobiology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX 77843, USA.
Recently, using a panel of recombinant CHO cell lines, we identified the coxsackie and adenovirus receptor (CAR) and histo-blood group antigens (HBGAs) or sialic acid as the minimum requirement for susceptibility to rhesus enteric calicivirus (ReCV) infections. While ReCVs cause lytic infection in LLC-MK2 cells, recombinant CHO (rCHO) cell lines did not exhibit any morphological changes upon infection. To monitor infectious virus production, rCHO cell cultures had to be freeze-thawed and titrated on LLC-MK2 monolayers.
View Article and Find Full Text PDFClin Genet
January 2025
Division of Pediatric Gastroenterology and Nutrition, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Coxsackie and adenovirus receptor-like membrane protein (CLMP) mutation is identified as a genetic risk factor of congenital short bowel syndrome (CSBS). However, the specific pathogenic mechanism remains unclear. This study aimed to explore the clinical manifestations, genetic characteristics, and molecular mechanisms underlying CSBS caused by CLMP mutations.
View Article and Find Full Text PDFMol Ther Oncol
December 2024
Department of Gene Therapy, Ulm University, 89081 Ulm, Germany.
Animals (Basel)
December 2024
Department of Preventive Medicine and Public Health, Semmelweis University, 1085 Budapest, Hungary.
Adenovirus (AdV) infection has been rarely documented in cats and other felids. Partial sequences of the hexon and fiber genes of a Hungarian feline adenovirus isolate (FeAdV isolate) showed a close relationship to human AdV (HAdV) type C1. Further molecular and biological characterization is reported here.
View Article and Find Full Text PDFNat 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 PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!