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  • 1
    Electronic Resource
    Electronic Resource
    The dual role of lymphocytic choriomeningitis virus-specific antibodies (1986)
    Springer
    Medical microbiology and immunology 175 (1986), S. 121-124 
    Details
    ISSN: 1432-1831
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02122430
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  • 2
    Electronic Resource
    Electronic Resource
    The effect of lymphocytic choriomeningitis virus-induced suppression of the delayed-type hypersensitivity reaction on virus clearance and pathogenicity (1986)
    Springer
    Medical microbiology and immunology 175 (1986), S. 129-131 
    Details
    ISSN: 1432-1831
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02122432
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    T-Cell Effector Function and Unresponsiveness in the Murine Lymphocytic Choriomeningitis Virus Infection (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 24 (1986), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: When the virus dose is increased from 102 (low dose) to 104 LD50 (high dose) a fatal lymphocytic choriomeningitis virus (LCMV) infection is changed into a subclinical one, and a selective virus-specific delayed-type hypersensitivity (DTH) unresponsiveness is induced, while the cytotoxic T-cell response remains essentially unchanged. When low-dose spleen effectors were transferred intravenously into intracerebrally infected high-dose mice, fatal LCM disease occurred, which means that infected central nervous system target structures in these animals are sensitive to virus-specific T cells. When low-dose cells were transferred to intravenously infected high-dose mice, these animals regained their TD function (the effect of T cells mediating DTH). Since this indicates that the survival of intracerebrally infected high-dose mice is intimately linked with the absence of virus-specific DTH reactivity, a search for T suppressor (Ts) activity in these animals was performed by transferring high-dose spleen cells to lethally (intracerebrally) infected low-dose recipients. In this way we obtained an afferent suppression, which was not H-2 restricted, but was abrogated when the spleen cells were pretreated with neutralizing anti-LCMV serum, indicating a suppressive effect of virus transferred with the infected cells. When tolerance induction was attempted with virus alone, a potentially fatal immune reaction could be altered to unresponsiveness (i.e. survival) as late as 4 days after an otherwise lethal infection with LCMV. The results indicate that the maturation of the virus-specific TD response is sensitive to large amounts of virus antigen. We conclude that this impairment and the resulting DTH unresponsiveness is due to a clonal deletion or anergy rather than to the effect of Ts cells, and that the TD effector function is critical to the development of fatal LCM disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1986.tb02078.x
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  • 4
    Electronic Resource
    Electronic Resource
    High-Dose Survival in the Lymphocytic Choriomeningitis Virus Infection Is Accompanied by Suppressed DTH but Unaffected T-Cell Cytotoxicity (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 21 (1985), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Provided that intracerebral inoculation is applied, an increase in the virus dose from 102to 104 LD50 of lymphocytic choriomeningitis virus (LCMV) leads to strikingly reduced mortality. To analyse the background for this autointerferencc, we measured several virologic and immunologic variables in mice infected with these doses of virus. In the high-dose mice we found generally higher organ virus titres and serum interferon titres than in the low-dose mice. Since we could demonstrate that virus-specific T-cell cytotoxicity in spleen, peripheral blood, and meningeal exudate was similar after intracerebral infection with large and small virus doses, and since the LCMV infection in the brain qualitatively and quantitatively was independent of the size of virus inoculum, the explanation for the survival of the high-dose animals is obviously not lack of possibilities for interaction between cytotoxic T cells and infected sensitive targets in the central nervous system. On the other hand, high doses of virus caused a clear suppression of the LCMV-specific delayed-type hypersensitivity(DTH). In addition, when splenocytes from high-dose animals were transferred either intravenously or locally into the footpad of newly virus-challenged mice. DTH was markedly suppressed as compared with the response after transfer of spleen cells from low-dose mice. We therefore conclude that autointerferencc in the LCMV infection is due to a selective suppression of Td function. Large amounts of persistent virus late after infection with high doses of virus suggest a central role for Td function also in virus clearance. Finally, our results indicate the existence of two subsets of K, D region-restricted T cells, one mediating cytotoxicity and the other mediating DTH. This possibility is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1985.tb01406.x
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  • 5
    Electronic Resource
    Electronic Resource
    The Combination of Major Histocompatibility Complex (MHC) and Non-MHC Genes Influences Murine Lymphocytic Choriomeningitis Virus Pathogenesis (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 29 (1989), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Resistance to the acute lethal disease caused by the docile strain of lymphocytic choriomeningitis (LCM) virus varies widely between different mouse strains. In order to study the inheritance of host influence on susceptibility to this strain of LCM virus, we crossed the F1 to the parent with the recessive disease phenotype. In all cases, susceptibility was dominant. In backcross progeny obtained from matings of parental strains differing in both major histocompatibility complex (MHC) and non-MHC (SWR; C3H), 90% of the challenged mice died, indicating that at least three loci controlled susceptibility to the disease. When the parental strains carried similar MHC haplotypes but dissimilar background genes (B10.BR; CBA), 78% of the backcross mice succumbed, indicating that at least two non-MHC loci influenced disease susceptibility. It is unlikely, however, that the same two non-MHC loci are critical in all genetic combinations, since F1 produced from two H-2 identical, resistant strains (B10.BR; C3H) were found to be fully susceptible. When congenic mice, differing only in the D-end of the MHC region, were analysed, 50% of the backcross animals died, indicating that one gene in the MHC region was important; segregation analysis comparing MHC serotype and disease outcome indicated the H-2D locus itself as the determining factor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1989.tb01155.x
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  • 6
    Electronic Resource
    Electronic Resource
    Different Tc Response Profiles are Associated with Survival in the Murine Lymphocytic Choriomeningitis Virus Infection (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 25 (1987), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The pathogenicity of lymphocytic choriomeningitis virus (LCMV) inoculated intracercbrally (i.e.) varies with virus sirain and dose as well as with the mouse strain used as host. Recently, results have indicated that susceptibility to lethal disease correlates directly with the ability of the host to produce early and high vinis-spccific Tc activity However, in the present studies we demonstrate that even though this holds true in many mouse/virus combinations, it does not apply in others Thus, in C3H mice infected with (moderately) high doses of Traub strain LCMV, early and high Tc activity was found despite a mortality rate of only 10–20%. Similarly. in C3H mice inoculated with the aggressive and docile suhstrains of UBC strain LCMV, which differ markedly in their pathogenicity for this mouse strain, similar kinetics of Tc induction were observed. Finally. in DBA/2 mice which do not die following infection with the otherwise lethal aggressive substrain. Tc induction could he found to be as efficient as m BALB/c mice, all of which die from acute LCM disease when infected with this virus isolate. The results indicate, therefore, that early and high Tc activiiy does not constitute a sufficient prerequisite for lethal disease. and that different Tc response profiles may he associated with low mortaility following i.e. inoculation with LCMV.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1987.tb01090.x
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  • 7
    Electronic Resource
    Electronic Resource
    Analysis of the Capacity to Produce IL-3 in Murine AIDS (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 40 (1994), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Adult C57BL/6 mice infected with LP-BM5 murine leukaemia virus represent a model of murine AIDS (MAIDS). In this study we have analysed the capacity of CD4+ T cells from infected mice to produce IL-3 following stimulation with ConA for 24–72 h. In contrast to the position with IL-2, the production of which is markedly impaired during LP-BM5 infection, similar levels of IL-3 were measured in culture supernatants of splenocytes from infected and uninfected mice harvested at 24 h of stimulation. Forty eight and 72 h of ConA stimulation led to increasing levels of IL-3 being measured in cultures from uninfected mice, whilst in cultures from infected animals, IL-3 levels remained stagnant. Similar results were obtained 4, 8 and 13 weeks post-infection. In view of the fact that parallel experiments revealed markedly impaired proliferative responses to ConA during MAIDS, we conclude that IL-3 production is basically intact at the cellular level in T cells during MAIDS; but when in a situation requiring clonal expansion of the activated T cells, IL-3 production will be inhibited owing to the impaired capacity for proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1994.tb03482.x
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  • 8
    Electronic Resource
    Electronic Resource
    T-Cell Effector Function and Unresponsiveness in the Murine Lymphocytic Choriomeningitis Virus Infection (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 24 (1986), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: An increase in the virus dose from 102 LD50 (low dose) to 104 LD50 (high dose) of lymphocytic choriomeningitis virus (LCMV) results in markedly delayed virus clearance, in spite of a potent cytotoxic T-cell (Tc) response. However, virus-specific delayed-type hypersensitivity (DTH) reactivity is markedly depressed in high-dose mice, suggesting an association between DTH and virus clearance. When virus-primed memory cells are transferred, DTH reactivity as well as virus-clearing capacity is restored in high-dose mice, indicating that the virus is not present in a changed or concealed form. The role of T-cells mediating DTH (TD cells) in virus clearance was also studied by adoptive transfer to naive recipients. Here the high-dose primed cells did mediate virus clearance, although no DTH reaction was detectable 24–72 h after transfer. However, when footpad swelling was measured 96 h or more after transfer a DTH response emerged, indicating that TD priming had taken place in high-dose animals. Pre-irradiation of high-dose primed cells markedly inhibited the antiviral activity as well as DTH, suggesting that upon transfer to naive recipients TD precursors from high-dose mice would proliferate into effector cells capable of mediating both functions. Treatment with anti-Lyt 2+C’ abrogated the capacity to induce virus-specific DTH, thus confirming that the cells involved are not helper T (TH) cells. We conclude that the DTH unresponsiveness in high-dose mice reflects a defective differentiation of TD precursor into effector cells which is reversible upon transfer to a less antigen loaded environment. Furthermore, it is suggested that TD function is crucial to the process of virus clearance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1986.tb02079.x
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  • 9
    Electronic Resource
    Electronic Resource
    The Susceptibility to Cytotoxic T Lymphocyte Mediated Lysis of Chemically Induced Sarcomas from Immunodeficient and Normal Mice (1997)
    Oxford, U.K. and Cambridge, USA : Blackwell Publishers
    Scandinavian journal of immunology 45 (1997), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A panel of sarcomas induced with 3-methylcholanthrene in normal and immunodeficient mice was studied for their capacity to present antigen by the endogenous, MHC class I restricted pathway. Lymphocytic choriomeningitis virus was used to infect cultured tumour cells, and the infected cells were tested for susceptibility to cytolysis by virus specific cytotoxic T cells. Tumour cells originating from tumours induced in immunocompetent C.B.-17 mice presented virus antigen more efficiently than tumour cells from immunodeficient SCID mice. No significant difference in virus antigen presentation was found between tumours from nude and nu/+ BALB/c mice. The sensitivity of target cells from the individual tumours to cytotoxic T lymphocyte (CTL) mediated lysis correlated negatively with their sensitivity to natural killer (NK) cell mediated lysis. There was a positive correlation between the sensitivity to CTL mediated lysis and surface expression of the MHC class I molecule Ld of the tumour cells. Tumour cells incapable of in vitro presentation of viral antigen to specific cytotoxic T cells originated from tumours known from previous experiments to be readily accepted after transplantation to immunocompetent, histocompatible recipients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1997.d01-369.x
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  • 10
    Electronic Resource
    Electronic Resource
    The Role of CD4+ T Cells in Cell-Mediated Immunity to LCM V: Studies in MHC Class I and Class II Deficient Mice (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 40 (1994), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Parameters of the virus-specific T-cell response were analysed in order to dissect the contribution of CD4+ and CDS+ T cells to cell-mediated immunity to lymphocytic choriomeningitis virus. In MHC class II deficient mice, initial T-cell responsiveness was not impaired, but virus clearance was delayed, and virus-specific Td activity declined more rapidly. Furthermore, class I restricted Tc memory appeared to be impaired in these mice. To directly evaluate the role of CD4+ cells in virus clearance and T-cell mediated inflammation, MHC class I deficient mice were also studied. No virus-specific delayed-type hypersensitivity reaction was detected following infection of the footpad, and only a few mice died from intracerebral challenge. However analysis of markers of T-cell activation as well as direct evaluation of CSF infiammation unveiled a low degree of T-cell activation and a chronic cellular exudate. This low-grade response was associated with some degree of virus control as organ titres were lower in these animals than in matched T-cell deficient nu/nu mice or class I deficient mice treated with anti-CD4 monoclonal antibody. This confirms that CD4+ cells are not needed to induce a virus-specific CD8+ T-cell response, but our findings strongly suggest that CD4+ T cells are critical for maintaining full antiviral immunity. Furthermore, CD4+ T cells per se have a low potential for mediating virus-specific infiammation that is associated with a low degree of virus control.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1994.tb03477.x
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