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Biomedical subjects

I McConnell

Publications and source records attributed to I McConnell.

131 records · Page 8Linked to original sources
PubMedDate not supplied

129/Ola mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal.

The neural membrane glycoprotein PrP is implicated in the pathogenesis of the transmissible spongiform encephalopathies; however, the normal function of PrP and its precise role in disease are not understood. Recently, gene targeting has been used to produce mice with neo/PrP fusion transcripts, but no detectable PrP protein in the brain (1). Here we report the use of a different targeting strategy, to produce inbred mice with a complete absence of both PrP protein and mRNA sequences. At 7 mo of age, these mice show no overt phenotypic abnormalities despite the normal high levels of expression of PrP during mouse development. The mice are being used in experiments designed to address the role of PrP in the pathogenesis of scrapie and the replication of infectivity.

Aging↗
PubMedDate not supplied

Interferon amplifies complement activation by Burkitt's lymphoma cells.

Interferon was originally described as an antiviral agent produced shortly after onset of infection with most viruses. However, in addition to inducing an antiviral state, interferon inhibits cell division, increases the expression of cell-surface antigens, boosts the cytotoxic activity of natural killer (NK) cells and modulates several immune functions of lymphocytes and macrophages. Moreover, a special class of interferon (immune interferon or IFN-gamma) is produced by T cells following stimulation with antigen or interaction with mitogens. The different methods by which interferon is induced and its multiple effects suggest that it may be part of a first-line defence system controlling the spread of virus infections and the proliferation of modified 'self' cells that have been affected by virus infection or neoplastic transformation. The ability of certain human lymphoma cells to activate the alternative pathway of complement is well established. Here we show that monoclonal antibody-purified interferon can amplify the ability of certain tumour cells to activate complement via the alternative pathway. This demonstration may reflect an additional, as yet unknown, role of interferon in inducing non-specific anti-tumour immunity.

Burkitt Lymphoma↗