PubMed:10092801 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/10092801","sourcedb":"PubMed","sourceid":"10092801","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/10092801","text":"Impaired fetal thymocyte development after efficient adenovirus-mediated inhibition of NF-kappa B activation.\nWe introduce a new experimental system combining adenovirus-mediated gene transfer and fetal thymic organ culture (FTOC). This system allowed us to efficiently express in developing thymocytes a mutant form of the NF-kappa B inhibitor I kappa B alpha (mut-I kappa B) and to study the maturation defects occurring when NF-kappa B activation is inhibited during fetal development. Fetal thymocytes infected with adenovirus containing mut-I kappa B were found to develop normally until the CD44-CD25+, CD4-CD8- double-negative stage, while production of more mature double-positive and single-positive populations was strongly decreased. Proliferation, as measured by the percentage of cells in cycle appeared normal, as did rearrangement and expression of the TCR beta-chain. However, apoptosis was much higher in FTOC infected with adenovirus containing mut-I kappa B than in FTOC infected with a control virus. Taken together, these results suggest that NF-kappa B plays a crucial role in ensuring the differentiation and survival of thymocytes in the early stages of their 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