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Biomedical subjects

J Lindenmann

Publications and source records attributed to J Lindenmann.

At least 37 records · Page 2Linked to original sources
PubMed1982

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.

History, 20th Century↗
PubMed1981

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.

Alleles↗
PubMed1981

[Perspectives in interferon research].

Progress in understanding of interferon-mediated mechanisms over the past 20 years has been steady although slow. A major obstacle has always been the difficulty of obtaining sufficient quantities of highly purified interferon. Rational therapeutic applications therefore depend on a solution of problems connected with mass production and purification of interferon.

Humans↗
PubMed1979

Natural, genetically determined resistance toward influenza virus in hemopoietic mouse chimeras. Role of mononuclear phagocytes.

Radiation chimeras produced by crosswise transfers of bone-marrow cell among histocompatible mice susceptible, or genetically resistant, to lethal challenge by a number of myxoviruses were used to test whether macrophage resistance (as assessed in vitro) and resistance of the animal (as measured in vivo), both previously shown to be brought about by the gene Mx, were causally related. 49 chimeras were tested individually, both of resistance of their macrophages to in vitro challenge with M-TUR (a strain of avian influenza virus A/Turkey/England/63 adapted to grow in cultured mouse peritoneal macrophages), and for resistance of the animal in vivo upon challenge with pneumotropic, neurotropic, or hepatotropic influenza viruses. Cultivated Kupffer cells and peritoneal macrophages harvested from chimeric mice expressed the resistance phenotype of the bone-marrow donor irrespective of the host environment in which they had differentiated. However, susceptibility or resistance in vivo was according to the genotype of the host. Thus, inborn resistance of radiation chimeras was found to be independent of Mx-gene expression in cells of the hemopoietic system.

Animals↗
PubMed1979

Genetically determined, interferon-dependent resistance to influenza virus in mice.

The genetically determined resistance towards orthomyxoviruses exhibited by mice homozygous (A2G) or heterozygous (A2G X A/J) for the gene Mx was abolished or greatly diminished by treatment with anti-interferon globulin (AIF). AIF induced increased susceptibility to challenge with hepatotropic, neurotropic, and pneumotropic strains of influenza A virus. Hepatotropic virus titers in blood and livers of AIF-treated, Mx-bearing mice were higher by a factor of 10(3)--10(6) than those in untreated mice of the same genotype, and were comparable to those in genetically susceptible (untreated or AIF-treated) mice. Peritoneal macrophages from Mx-bearing untreated mice were resistant to challenge with a macrophage-adapted strain of influenza A virus even in the presence of AIF. However, when macrophages were taken from resistant mice injected with AIF and also cultivated in the presence of AIF, they were as susceptible to the virus as macrophages taken from susceptible mice. We conclude that interferons is an important factor in resistance to orthomyxoviruses governed by the gene Mx.

Animals↗
PubMed1979

Alloantigens derived from stimulator cells and bound onto MLC-activated rat T lymphoblasts.

Rat T lymphocytes were activated in MLC (mixed leucocyte culture) against allogeneic stimulator cells. A few percent of such T blasts could be shown to carry IgM on their surface when a mixture of T and B lymphocytes was used as responder cells. The immunoglobulin was absent when purified T lymphocytes served as responders. A large proportion of MLC T lymphoblasts could be shown to carry stimulator alloantigens on their surface. These antigens were demonstrated (a) by indirect immunofluorescence using anti-stimulator alloantibody and FITC (fluorescein isothiocyanate Isomer I)-labelled F(ab)2 fragments of rabbit anti-rat Ig; (b) by autoradiography after internal labelling of stimulator cells, which showed the transfer of label from stimulator to responder cells. For biochemical analysis T blasts were restimulated with internally labelled allogeneic or syngeneic stimulator cells, and bound radiolabelled stimulator alloantigens were analysed on SDS-PAGE (sodium lauryl sulphate polyacrylamide gel electrophoresis). The results suggest that intact SD antigens with a molecular weight of 45,000 daltons and LD determinants with a molecular weight of 34,000 daltons derived from stimulator cells are found on MLC T blasts. No evidence of binding of the 27,000-dalton Ia chain to T blasts was found. Possible arrangements of these molecules on the responder blasts is discussed.

Animals↗
PubMed1978

Inborn resistance of mice to myxoviruses: macrophages express phenotype in vitro.

A strain of avian influenza A virus was adapted to grow in mouse peritoneal macrophages in vitro. The adapted strain, called M-TUR, induced a marked cytopathic effect in macrophages from susceptible mice. Mice homozygous (A2G) or heterozygous (F1 hybrids between A2G and several susceptible strains) for the gene Mx, shown previously to induce a high level of resistance towards lethal challenge by a number of myxoviruses in vivo, yielded peritoneal macrophages which were not affected by M-TUR. Peritoneal macrophages could be classified as resistant or susceptible to M-TUR without sacrificing the cell donor. Backcrosses were arranged between (A2G X A/J)F1 and A/J mice. 64 backcross animals could be tested individually both for resistance of their macrophages in vitro after challenge with M-TUR, and for resistance of the whole animal in vivo after challenge with NWS (a neurotropic variant of human influenza A virus). Macrophages from 36 backcross mice were classified as susceptible, and all of these mice died after challenge. Macrophages from 28 mice were classified as resistant, and 26 mice survived challenge. We conclude that resistance of macrophages and resistance of the whole animal are two facets of the same phenomenon.

Alleles↗