TY - JOUR
T1 - Increase of vulnerability to lymphotoxin in cells infected by vesicular stomatitis virus and its further augmentation by interferon
AU - Aderka, D.
AU - Novick, D.
AU - Hahn, T.
AU - Fischer, D. G.
AU - Wallach, D.
N1 - Funding Information:
i This study was supported by a grant from the Fund of Basic Research, administered by the Israel Academy of Sciences and Humanities and by a grant from the Leukemia Research Foundation, Chicago, Ill. * To whom correspondence should be addressed. 3 Abbreviations used: CHI-cycloheximide; IFN-interferon; LT-lymphotoxin; PFU-plaque forming unit; PHA-phytohemagglutinin; VSV-Vesicular Stomatitis Virus.
PY - 1985/5
Y1 - 1985/5
N2 - The cytotoxic effect of lymphotoxin (LT) and its modulation by interferon (IFN) was quantitatively assessed in uninfected and vesicular stomatitis virus (VSV)-infected cultured cells. Preparations of human LT, which were depleted of IFN, had a significant cytotoxic effect on VSV-infected HeLa, SV-80, WISH, and Vero cells. IFN, most notably IFN-γ, further potentiated destruction of the infected cells by these LT preparations, when applied on the cells at sub-antiviral IFN concentrations. In contrast, no cytotoxic effect could be observed in any of the examined cells, when applying LT, IFN, or their combination, in the absence of viral infection. Infected cells in which VSV replication was suppressed by treatment with antiviral concentrations of IFN also resisted destruction by LT. These findings indicate that LT cytotoxicity can be selectively directed against virus-infected cells and that IFN can augment this cell-killing mechanism when failing to exert an antiviral effect.
AB - The cytotoxic effect of lymphotoxin (LT) and its modulation by interferon (IFN) was quantitatively assessed in uninfected and vesicular stomatitis virus (VSV)-infected cultured cells. Preparations of human LT, which were depleted of IFN, had a significant cytotoxic effect on VSV-infected HeLa, SV-80, WISH, and Vero cells. IFN, most notably IFN-γ, further potentiated destruction of the infected cells by these LT preparations, when applied on the cells at sub-antiviral IFN concentrations. In contrast, no cytotoxic effect could be observed in any of the examined cells, when applying LT, IFN, or their combination, in the absence of viral infection. Infected cells in which VSV replication was suppressed by treatment with antiviral concentrations of IFN also resisted destruction by LT. These findings indicate that LT cytotoxicity can be selectively directed against virus-infected cells and that IFN can augment this cell-killing mechanism when failing to exert an antiviral effect.
UR - http://www.scopus.com/inward/record.url?scp=0021799201&partnerID=8YFLogxK
U2 - 10.1016/0008-8749(85)90003-6
DO - 10.1016/0008-8749(85)90003-6
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AN - SCOPUS:0021799201
SN - 0008-8749
VL - 92
SP - 218
EP - 225
JO - Cellular Immunology
JF - Cellular Immunology
IS - 2
ER -