Cell-mediated cytotoxicity against Sendai-virus-infected cells (original) (raw)
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European Journal of Immunology, 1980
Virus-specific T cell induction in vitro 715 m i c h H-Koszinowski and Markus M. Generation of virus-specific cytotoxic T cells in vitro I. Induction conditions of primary and secondary Sendai virus-specific cytotoxic T cells* Simon Institut fur Immunologie und Genetik, Deutsches Krebsforschungszentrum, Heidelberg H-Zrestricted cytotoxic T cells specific for Sendai virus were generated in vitro in a primary response from normal mouse lymphocytes cultured in the presence of infective as well as inactivated Sendai virus. Antigen-presenting cells of different origin, including T cells, were found to be effective stimulators. Antibodies to Sendai virus were shown to inhibit the activation of specific precursor killer cells when added to cultures before, but not after, the addition of viral antigen. Data obtained by Lyt phenotyping, revealed that precursor killer cells specific for Sendai virus reside in the Lyt-2,3+ T cell population and that Lyt-1,2,3+ T cells are not required for the generation of cytotoxic lymphocytes. Different activation kinetics were demonstrated for primary and secondary antiviral cytotoxic responses, and the analysis of the proliferation and stimulation requirements suggests qualitative differences.-70 "C. 2.3 Immunization * Supported by the Deutsche Forschungsgemeinschaft KO 571/6.
The cytotoxic T-lymphocyte response to Sendai virus is unimpaired in the absence of gamma interferon
Journal of Virology, 1997
Sendai virus is eliminated from the respiratory tract of gamma interferon (IFN-␥) ؊/؊ BALB/c mice with normal kinetics. The level of virus-specific cytotoxic T-lymphocyte (CTL) activity in the cell population recovered by bronchoalveolar lavage is unimpaired, the prevalence of interleukin-4 (IL-4)-producing cells is increased, and the titers of virus-specific immunoglobulins IgG1 and IgG2b are higher in the IFN-␥ ؊/؊ mice. The emergence of this T-helper 2 response profile in both lymphoid tissue and the pneumonic lung has no obvious deleterious consequences. Virus clearance is slightly delayed following depletion of the CD4 ؉ subset, with the effect being similar in magnitude for IFN-␥ ؊/؊ and ؉/؉ mice. However, the generation of CTL precursors (CTLp) is diminished in the IFN-␥ ؊/؊ (but not ؉/؉) mice in the absence of concurrent CD4 ؉ T help. Apparently the clonal expansion of the CTLp population can be promoted either by a cytokine (perhaps IL-2) produced by the IFN-␥ ؊/؊ CD4 ؉ T cells or by IFN-␥ made by other cell types in the ؉/؉ mice.
Tumor necrosis factor induction by Sendai Virus
The Journal of Immunology
Supernatants of peripheral blood mononuclear leukocytes (PBMC) treated with Sendai virus were found to exert significant cytotoxic effects mediated by leukocyte-produced proteins distinct from interferon. Fractionation of the PBMC into adherent and nonadherent cells indicated that these virus-induced cytotoxins (CTX) were produced primarily in the mononuclear phagocytes. Cells of the rnonocytelike U937 line pretreated with 4B-phorbol-12-myristate-13-acetate could also be induced with Sendai virus to produce CTX. The nonadherent mononuclear cells of the peripheral blood responded poorly to the virus with regard to CTX production, even though they could be induced to produce CTX with phytohemagglutinin (PHA). With the use of monospecific antibodies to tumor necrosis factor (TNF) and to lymphotoxin (LT), it was found that TNF is the major CTX produced by PBMC and by the U937 cells after 24 hr stimulation by the virus, whereas LT is not induced under these conditions to any measurable extent. TNF was also found to be produced in significant amounts together with LT upon stimulation of the nonadherent fraction of the PBMC by PHA. These findings indicate that besides bacterial lypopolysaccharides, other biological agents including viruses can be effective inducers of tumor necrosis factor, suggesting implications regarding the physiologic role of this protein.
Journal of Experimental Medicine, 1986
The in vivo importance of class I MHC regulation of the Tc response to a natural pathogenic agent of high virulence was studied on the basis of our previous demonstration of a major difference in the capacity to generate a Sendai virus-specific Tc response between C57BL/6 (B6, H-2b) mice and H-2Kb mutant B6.C-H-2bm1 (bm 1) mice. These two mouse strains differ from each other only in three amino acids in the crucial H-2Kb restriction element for this response. bm 1 mice, in contrast to B6 mice, are Tc nonresponders against this virus, but show Sendai-specific T cell proliferation, antibody production, and DTH reactions, as well as NK cell activity, equal to those of B6 mice. B6, Sendai Tc-deficient bm 1 and T cell-deficient B6 nu/nu mice differ from each other in susceptibility to lethal pneumonia induced by i.n. inoculation of virulent Sendai virus. The lethal dose (LD50) in B6 mice averaged 152 TCID50, in bm 1 mice, 14 TCID50 and in B6 nu/nu mice 0.5 TCID50. The importance of Tc wa...
Gross-virus-induced lymphoma in the rat. IV. Cytotoxic cells in normal rats
International Journal of Cancer, 1977
Lymphoid cells from normal W/Fu rats are cytotoxic in vitro for syngeneic Gross-virus-induced lymphoma cells in a 4% h 51Cr release test, and protect against tumour growth in vivo when adoptively transferred to syngeneic recipient rats. Cytotoxicity by normal lymphoid cells was greater with in vitro rather than in vivo passaged target cells. and was increased by preincubation of the lymphoid cells at 37-C for 3 h in vitro before their addition to the target cells. Cytotoxlc activity, which was localized predominantly in the spleen, was absent at birth but increased until adulthood with some decline in older age. Histocompatibility at the major Ag-B locus was not required for the killer cell-target cell interaction; normal spleen cells of many Ag-B genotypes were cytotoxic for W/FuG-1 target cells, although B D l X and (B D I X x W/Fu)Fl were less active and B N were inactive. The specificity of cytotoxicity was studied by the techniques of direct lysis, competitive inhibition or adsorption to cellular monolayers, using a variety of cell lines. Selectively of lysis or binding was observed and was restricted to rat target cells releasing exogenous or endogenous C-type viruses. Cell-mediated anti-tumour responses following tumour implantation have been described for a