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  • 1
    Electronic Resource
    Electronic Resource
    Dissociation of Autoaggression and Self-Superantigen Reactivity (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 37 (1993), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Self-superantigens have been described as products of endogenous retroviruses of the mouse (‘minor lymphocyte stimulating loci’) that are capable of interacting without prior processing with conserved domains of TCR Vβ chains, causing the activation and deletion of most T cells expressing products of determined Vβ gene families [1–4], The fact that superanti-gens activate a far higher percentage of T cells (1–20%) than conventional, peptidic antigens (〈 0.1 %) provides the methodological advantage that the degree of clonal deletion may be measured by the analysis of the TCR repertoire using appropriate anti-Vβ antibodies. Although much information on the spatio-temporal organization of repertoire-purging has been gathered by virtue of self-superantigens, serious doubts exist as to the possibility that such structures serve as pathogenetically relevant autoantigens. Thus, certain inbred mice spontaneously develop autoimmune diseases, although they bear T-cell repertoires that appear to be purged from self-superantigen-reactive Vβ products. In addition, therapeutic interventions targeted to Vβ gene products that are not specific for self-superantigens are successful in preventing disease development. The lack of correlation between superantigen-related Vβ deletions and autoimmune disease development is substantiated in further models of murine autoimmunity. Based on these observations, we formulate the hypothesis that self-superantigen-reactive T cells are not involved in the development of autoimmune diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1993.tb01657.x
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  • 2
    Electronic Resource
    Electronic Resource
    CD4-targeted immune intervention: a strategy for the therapy of AIDS and autoimmune disease
    Amsterdam : Elsevier
    Trends in Biotechnology 9 (1991), S. 124-131 
    Details
    ISSN: 0167-7799
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0167-7799(91)90043-H
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  • 3
    Electronic Resource
    Electronic Resource
    Highly Efficient Expression of Proteins Encoded by Recombinant Vaccinia Virus in Lymphocytes (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 34 (1991), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Using a recombinant vaccinia virus (VV) that expresses E. coli β galactosidase (β-Gal) to infect lymphocytes, we show that enzymometrically or immunologically detectable β-Gal expression is less pronounced among T cells than among B cells, VV infection caused growth inhibition of B cells, but barely affected T-cell proliferation in vitro. Moreover, the production of infectious viral particles was less pronounced in T lymphocytes. Kinetic studies revealed that after an initial dose-dependent growth inhibition, T cells continued to proliferate without the doubling time being affected by VV infection. Nonetheless. The T cells do express proteins encoded by recombinant VV. such β-Gal. or secrete soluble proteins such as interleukin-4, though at a lower efficiency at the per cell level than B lymphocytes. In conclusion, the physiology of T cells appears lo be less perturbed by VV than that of B ceils, although the virus is capable of directing expression of recombinant genes to T lymphocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1991.tb01585.x
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  • 4
    Electronic Resource
    Electronic Resource
    Isotope shifts in the atomic spectrum of xenon and nuclear deformation effects (1974)
    Springer
    The European physical journal 270 (1974), S. 113-120 
    Details
    ISSN: 1434-601X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract Optical isotope shifts of four lines in the atomic spectrum of xenon have been measured using enriched samples of all stable xenon isotopes. The spectrograms were recorded with the aid of a pressure-scanned Fabry-Pérot interferometer and analysed by digital data techniques. The measured isotope shifts are shown to be self-consistent by means of a King plot. An estimate of the specific mass effect is given and the changesδ 〈r 2〉 of the mean square radius of the nuclear charge distribution are extracted from the measured shifts. These changesδ 〈r 2〉 are discussed in terms of the nuclear deformation parameterβ 2. The results for the deformation of the stable even xenon isotopes are shown to be in good agreement with the systematic of deformation found for the neighbouring elements from Coulomb excitation experiments.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01677442
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  • 5
    Electronic Resource
    Electronic Resource
    Pathophysiology of mitochondrial cell death control (1999)
    Springer
    Cellular and molecular life sciences 56 (1999), S. 971-976 
    Details
    ISSN: 1420-9071
    Keywords: Key words. apoptosis; necrosis; permeability transition.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Mitochondria have been recently recognized to play a major role in the control of apoptosis or programmed cell death. Permeabilization of mitochondrial membranes, a decisive feature of early cell death, is regulated by members of the Bcl-2 family which interact with the permeability transition pore complex (PTPC). Thus, the cytoprotective oncoprotein Bcl-2 stabilizes the mitochondrial membrane barrier function, whereas the tumor suppressor protein Bax permeabilizes mitochondrial membranes. The regulation of membrane permeabilization is intertwined with that of the bioenergetic and redox functions of mitochondria. The implications of alterations in the composition of the PTPC and in mitochondrial function for the pathophysiology of cancer (reduced apoptosis) and neurodegeneration (enhanced apoptosis) are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000180050486
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  • 6
    Electronic Resource
    Electronic Resource
    ev22, a new endogenous avian leukosis virus locus found in chickens with spontaneous autoimmune thyroiditis (1988)
    Springer
    Archives of virology 100 (1988), S. 267-271 
    Details
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Chickens of the Obese strain (OS) develop a hereditary spontaneous autoimmune thyroiditis (SAT) which closely resembles human Hashimoto's disease. Analysis of the endogenous viruses harboured by these animals revealed a new endogenous virus (ev22) detected as a 5.5kb Sac I fragment. Crossbreeding experiments showed thatev22 is vertically transmitted as an autosomal trait not associated with major histocompatibility (MHC) alleles. Preliminary experiments indicate thatev22 does not necessarily cause SAT, however, it may have a modulatory role in the development of the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01487689
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  • 7
    Electronic Resource
    Electronic Resource
    The cell biology of apoptosis: Evidence for the implication of mitochondria (1996)
    Springer
    Apoptosis 1 (1996), S. 231-242 
    Details
    ISSN: 1573-675X
    Keywords: Bcl-2 ; mitochondrial transmembrane potential ; permeability transition ; proteases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The apoptotic process can be subdivided into three phases: a death-stimulus-dependent heterogeneous induction phase, a common effector phase during which the central apoptotic executioner is activated, and a common degradation phase during which cells acquire the biochemical and morphological features of end-stage apoptosis. Recently, it has become clear that the central apoptosis executioner is dictated by cytoplasmic (non-nuclear) events and that nuclear changes that define apoptosis (chromatin condensation and oligonucleosomal DNA fragmentation) only become manifest beyond the point-of-no-return of apoptosis, during the late degradation phase. It appears that one obligatory event of the apoptotic cascade involves a characteristic change in mitochondrial function, namely the so-called mitochondrial permeability transition. Permeability transition leading to disruption of the mitochondrial transmembrane potential precedes nuclear and plasma membrane features of apoptosis. Induction of permeability transition in cells suffices to cause the full-blown picture of apoptosis. In vitro induction of permeability transition in isolated mitochondria provokes the release of a factor capable of inducing apoptotic changes in isolated nuclei. Permeability transition is subject to regulation by multiple endogenous effectors, including members of the bcl-2 gene family. Its inhibition by pharmacological agents or hyperexpression of Bcl-2 prevents apoptosis, indicating that PT is a central coordinating event of the apoptotic effector stage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00143316
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  • 8
    Electronic Resource
    Electronic Resource
    Palmitate induces apoptosis via a direct effect on mitochondria (1999)
    Springer
    Apoptosis 4 (1999), S. 81-87 
    Details
    ISSN: 1573-675X
    Keywords: Bcl-2 ; carnitine ; fatty acids ; mitochondrial megachannel ; permeability transition pore.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The fatty acid palmitate can induce apoptosis. Here we show that the palmitate-induced dissipation of the mitochondrial transmembrane potential (ΔΨ m ), which precedes nuclear apoptosis, is not prevented by inhibitors of mRNA synthesis, protein synthesis, caspases, or pro-apoptotic ceramide signaling. However, the mitochondrial and nuclear effects of palmitate are inhibited by overexpression of anti-apoptotic proto-oncogene product Bcl-2 and exacerbated by 2-bromo-palmitate as well as by carnitine. The cytoprotective actions of Bcl-2, respectively, is not antagonized by etomoxir, an inhibitor of carnitine palmitoyl transferase 1 (CPT1), suggesting that the recently described physical interaction between CPT1 and Bcl-2 is irrelevant to Bcl-2-mediated inhibition of palmitate-induce apoptosis. When added to purified mitochondria, palmitate causes the release of soluble factors capable of stimulating the apoptosis of isolated nuclei in a cell-free system. Mitochondria purified from Bcl-2 over-expressing cells are protected against the palmitate-stimulated release of such factors. These data suggest that palmitate causes apoptosis via a direct effect on mitochondria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009694124241
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  • 9
    Electronic Resource
    Electronic Resource
    Apoptosis of cells lacking mitochondrial DNA (1996)
    Springer
    Apoptosis 1 (1996), S. 119-125 
    Details
    ISSN: 1573-675X
    Keywords: Mitochondrial transmembrane potential ; permeability transition ; programmed cell death ; reactive ; oxygen species
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The mitochondrial genome of animals encodes a few subcomponents of the respiratory chain complexes I, III and IV, whereas nuclear DNA encodes the overwhelming majority, both in quantitative and qualitative terms, of mitochondrial proteins. Complete depletion of mitochondrial DNA (mtDNA) can be achieved by culturing cells in the presence of inhibitors of mtDNA replication or mitochondrial protein synthesis, giving rise to mutant cells (ϱ∘ cells) which carry morphological near-to-intact mitochondria with respiratory defects. Such cells can be used to study the impact of mitochondrial respiration on apoptosis. ϱ∘ cells do not undergo cell death in response to determined stimuli, yet they conserve their potential to undergo full-blown apoptosis in many experimental systems. This indicates that mtDNA and associated functions (in particular mitochondrial respiration) are irrelevant to apoptosis execution. However, the finding that mtDNA-deficient mitochondria can undergo apoptosis does not argue against the involvement of mitochondria in the apoptotic process, since mitochondria from ϱ∘ cells conserve most of their functions including those involved in the execution of the death programme: permeability transition and release of one or several intermembrane proteins causing nuclear apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01321017
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  • 10
    Electronic Resource
    Electronic Resource
    Mitochondrial permeability transition in apoptosis and necrosis (1998)
    Springer
    Cell biology and toxicology 14 (1998), S. 141-145 
    Details
    ISSN: 1573-6822
    Keywords: mitochondrial transmembrane potential ; permeability transition ; programmed cell death ; proteases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Apoptosis has classically been viewed as a process not involving mitochondria, whereas the implication of mitochondrial dysfunction in necrosis has been recognized for several decades. Recently, it has become clear that apoptosis implies a disruption of mitochondrial membrane intregrity that is decisive for the cell death process. Cytofluorometric methods assessing the mitochondrial membrane function and structure can be employed to demonstrate that, at least in most models of apoptosis, mitochondrial changes precede caspase and nuclease activation. Moreover, pharmacological and genetic experiments suggest that the loss of mitochondrial membrane integrity is a critical event of the apoptotic process, beyond or at the point of no return of programmed cell death. Inhibitors of the mitochondrial megachannel (= permeability transition pore) can prevent both the mitochondrial and the post-mitochondrial manifestations of apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007486022411
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