Biomedical subjects
J Lindenmann
Publications and source records attributed to J Lindenmann.
The National Institute for Medical Research, Mill Hill. Personal recollections from 1956/57.
Explore the source record for details and available documents.
[Transgressing the limits of naturopathy].
Three examples of the tendency of nonconventional medicine to transgress its self-imposed limits are presented: (1) the efforts of Benveniste to confer scientific respectability on homeopathy; (2) the attempt, by press conference, to popularize home delivery; (3) the creation of a new demand by the offer of subaquatic delivery.
Duesberg on AIDS--stretching our benevolence beyond its limits.
Explore the source record for details and available documents.
[The contribution of virology to medicine, biology and molecular biology].
Explore the source record for details and available documents.
[Give credit where credit is due?].
Explore the source record for details and available documents.
[Interferon or the long walk].
Explore the source record for details and available documents.
[AIDS--economics and ecology].
Explore the source record for details and available documents.
[Virus-host relations: from confrontation to peaceful coexistence].
Explore the source record for details and available documents.
Virus interference. I. The interferon. By A. Isaacs and J. Lindenmann, 1957.
Explore the source record for details and available documents.
Mx protein: constitutive expression in 3T3 cells transformed with cloned Mx cDNA confers selective resistance to influenza virus.
Mx+ mice are much more resistant to influenza virus than Mx- strains. The resistance is mediated by interferon (IFN) alpha/beta. After IFN treatment, Mx+ but not Mx- cells accumulate Mx protein and become specifically resistant to orthomyxoviruses. cDNA encoding Mx protein was cloned and sequenced. Southern analyses indicate that Mx- alleles derive from their Mx+ counterpart by deletions. IFN-treated Mx+ cells contained a 3.5 kb Mx mRNA, while Mx- cells showed only traces of shorter Mx RNA. Mx- cells transformed with Mx cDNA expressed Mx protein constitutively to varying extents; resistance of individual cells to influenza virus correlated with Mx protein expression. Thus, specific resistance to influenza virus in vivo may be attributed to Mx protein expression and is independent of other IFN-mediated effects.
Interferon-regulated influenza virus resistance gene Mx is localized on mouse chromosome 16.
Genomic Southern blots of mouse-hamster somatic cell hybrids were analyzed with a probe prepared from a cDNA encoding murine Mx protein, the product of the interferon-regulated influenza virus resistance allele Mx+. Results of this analysis indicate that the Mx gene is located on mouse chromosome 16. In appropriate backcross mice, no linkage was observed between Mx and md, a marker previously mapped close to the centromere of chromosome 16, suggesting a more distal localization of Mx.
Polyclonal and monoclonal antibodies to the interferon-inducible protein Mx of influenza virus-resistant mice.
Interferon-alpha/beta induces in cells from mice carrying the influenza virus resistance allele Mx+ the synthesis of a unique 75,000-dalton protein (designated here protein Mx) that was not detectable in interferon-treated cells from Mx- mice lacking the resistance allele (Horisberger, M. A., Staeheli, P., and Haller, O. (1983) Proc. Natl. Acad. Sci. U. S. A. 80, 1910-1914). We have immunized Mx- BALB/c mice with extracts of interferon-treated cells from congenic Mx+ BALB X A2G-Mx mice. Resulting hyperimmune sera immunoprecipitated a single interferon-inducible 75,000-dalton protein of Mx+ embryo cells. Sera did not react with any interferon-inducible protein of Mx- cells. Synthesis of the immunoprecipitable 75,000-dalton protein Mx was induced by interferon-alpha/beta but not by interferon-gamma in Mx+ cells of diverse genetic backgrounds. Monoclonal antibodies to protein Mx were selected in similar immunoprecipitation assays. One discrete in vitro translation product of relevant mRNA reacted with polyclonal and monoclonal antibodies and was indistinguishable from in vivo synthesized protein Mx.
Origin of the terms 'antibody' and 'antigen'.
Explore the source record for details and available documents.
[Vaccines: immunologic principles].
Explore the source record for details and available documents.
From interference to interferon: a brief historical introduction.
The idea that a substance mediating interference was released from cells upon contact with inactivated influenza A virus emerged from an abortive attempt at showing that interference was initiated by passage of only part of the virus into the cell, from previous knowledge about interference, and from the use of a simple technique allowing easy separation of fluid and tissue.
Virus-specific interferon action. Protection of newborn Mx carriers against lethal infection with influenza virus.
The efficacy of interferon in antiviral protection of newborn mice differing at the Mx locus was investigated. Adult mice bearing the allele Mx exhibit a high degree of specific resistance toward lethal challenge with influenza viruses. In contrast, newborn Mx carriers are virtually as susceptible to influenza viruses as newborn mice devoid of Mx. Resistance can be abrogated by treating adult animals with anti-interferon serum. Here, we provide direct evidence of a virus-specific effect of interferon in vivo: newborn mice carrying the resistance gene Mx could be protected against lethal influenza virus infection with doses of interferon that were not protective in the absence of Mx. The efficacy of interferon towards a picornavirus (encephalomyocarditis virus) and a rhabdovirus (vesicular stomatitis virus) was independent of Mx.