Metabolic requirements for the in vitro augmentation of mouse natural killer activity by interferon

Djeu, Julie Y.; Stocks, Naomi I.; Varesio, Luigi; Holden, Howard T.; Herberman, Ronald B.

doi:10.1016/0008-8749(81)90148-9

Cited by 35 publications

(18 citation statements)

References 20 publications

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“…They also lyse cells infected with certain viruses, thereby inhibiting further viral replication and spread of infection (1). Treatment of mice or humans with poly(I:C) or stimulation of PBMC cultures in vitro resulted in higher cytotoxic activity (31)(32)(33)(34). This activation was thought to be mediated by IFN-␣ produced by activated DCs or macrophages (31)(32)(33)(34).…”

Section: Poly(i:c) Stimulation Enhances Nk Cell Cytotoxicitymentioning

confidence: 99%

“…Treatment of mice or humans with poly(I:C) or stimulation of PBMC cultures in vitro resulted in higher cytotoxic activity (31)(32)(33)(34). This activation was thought to be mediated by IFN-␣ produced by activated DCs or macrophages (31)(32)(33)(34). Similarly, the combination of IL-2 and poly(I:C) was shown to increase cytotoxic activity of PBMC (35,36).…”

Section: Poly(i:c) Stimulation Enhances Nk Cell Cytotoxicitymentioning

confidence: 99%

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APC-Independent Activation of NK Cells by the Toll-Like Receptor 3 Agonist Double-Stranded RNA

Schmidt¹,

Leung²,

Kwong³

et al. 2004

The Journal of Immunology

219

167

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Toll-like receptors (TLRs) play a fundamental role in the recognition of bacteria and viruses. TLR3 is activated by viral dsRNA and polyinosinic-polycytidylic acid (poly(I:C)), a synthetic mimetic of viral RNA. We show that NK cells, known for their capacity to eliminate virally infected cells, express TLR3 and up-regulate TLR3 mRNA upon poly(I:C) stimulation. Treatment of highly purified NK cells with poly(I:C) significantly augments NK cell-mediated cytotoxicity. Poly(I:C) stimulation also leads to up-regulation of activation marker CD69 on NK cells. Furthermore, NK cells respond to poly(I:C) by producing proinflammatory cytokines like IL-6 and IL-8, as well as the antiviral cytokine IFN-γ. The induction of cytokine production by NK cells was preceded by activation of NF-κB. We conclude that the ability of NK cells to directly recognize and respond to viral products is important in mounting effective antiviral responses.

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Section: Poly(i:c) Stimulation Enhances Nk Cell Cytotoxicitymentioning

confidence: 99%

Section: Poly(i:c) Stimulation Enhances Nk Cell Cytotoxicitymentioning

confidence: 99%

APC-Independent Activation of NK Cells by the Toll-Like Receptor 3 Agonist Double-Stranded RNA

Schmidt¹,

Leung²,

Kwong³

et al. 2004

The Journal of Immunology

219

167

View full text Add to dashboard Cite

show abstract

“…Trinchieri et al (9), presented some evidence for IF production by NK cells themselves, in response to tumor cells in vitro. However, macrophages appeared to be the main source of IF (19) by poly inosinic:poly cytidylic acid boosting of mouse NK activity. Similarly, macrophages are required in the Bacille Calmette-Gu~rin boosting of NK activity (6).…”

Section: Discussionmentioning

confidence: 92%

Augmentation of mouse natural killer activity and induction of interferon by tumor cells in vivo.

Djeu¹,

Huang²,

Herberman³

1980

The Journal of Experimental Medicine

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Conventional and nude mice inoculated with syngeneic or allogenic tumor cells developed a rapid rise in serum interferon (IF) levels, peaking within 24 h. Within the same period, natural killer (NK) activity was readily boosted in the spleen. Both activities usually declined at 3 d. Cells that lacked the ability to augment NK activity also failed to induce detectable levels of IF. The boosting of IF and NK functions did not appear to be a result of contamination of the tumor lines by viruses because inoculation of several type C viruses into normal mice had no effect, and other viruses, like lymphocytic choriomeningitis virus and influenza, elevated IF and NK levels with a significantly later kinetics, peaking 3-4 d. The IF induced by tumor cells was heat and acid labile, species specific, and appeared to be in the type II class, although it was susceptible to antisera against Newcastle disease virus-induced IF. These data suggest that an early, nonthymus-dependent consequence of tumor-cell recognition is the production of IF, which, in turn, activates NK cells to lyse the tumor cells.

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“…Macrophage-related cell lines also produce interferon if they are treated with inducing agents (4,20). In the present study, large quantities of interferon were produced by cells that have macrophage properties and that were cultivated by the second (BP) method, when they were stimulated by LPS, OK-432, or poly(I)· poly(C) (Fig.…”

Section: Discussionmentioning

confidence: 99%

Production of Interferon by an SV40‐Transformed Macrophage Line, BB‐W‐531–2

Takayama

Tanigawa

Takagi

1981

Microbiology and Immunology

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A simian virus 40-transformed mouse macrophage line, BB-W-531-2, was examined for its ability to produce interferon. BB-W-531-2 cells showed a phenotypic change between the macrophage and the nonmacrophage states. A viral inhibitor (interferon) was produced by the cells during the phenotypic change from the nonmacrophage to the macrophage state. Cells having macrophage properties were well capable of producing interferon when they were stimulated with ultraviolet-inactivated vaccinia virus, lipopolysaccharide, a streptococcal preparation (OK-432) or polyinosinate . polycytidylate. In contrast, cells that had lost their macrophage properties did not produce interferon even when they were given the same treatments as the cells having macrophage properties. The results suggest that the ability of BB-W-531-2 cells to produce interferon is associated with the expression of several macrophage properties.

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Metabolic requirements for the in vitro augmentation of mouse natural killer activity by interferon

Cited by 35 publications

References 20 publications

APC-Independent Activation of NK Cells by the Toll-Like Receptor 3 Agonist Double-Stranded RNA

APC-Independent Activation of NK Cells by the Toll-Like Receptor 3 Agonist Double-Stranded RNA

Augmentation of mouse natural killer activity and induction of interferon by tumor cells in vivo.

Production of Interferon by an SV40‐Transformed Macrophage Line, BB‐W‐531–2

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